Scottish Doctor, author, speaker, sceptic

What causes heart disease – part 59

A number of people have written to me asking how to read all the articles I have written on cardiovascular disease. I understand it is not exactly easy to do this. So, here I am going to attempt a short summary of everything I have written up to now.

Thrombogenic theory vs. LDL/cholesterol hypothesis

Since the mid-nineteenth century there have been two main, and almost entirely conflicting, hypotheses as to what causes cardiovascular disease. At present it may seem as if there is only one, the cholesterol or LDL hypothesis. Namely that a raised low-density lipoprotein is the underlying/primary/necessary cause.

I am not running through all the reasons why this hypothesis is wrong here. I will confine myself to one simple point. For the LDL hypothesis to be correct, it requires that LDL can travel past the lining of the artery, the endothelial cells, and into the artery wall behind. This is considered the starting point for atherosclerotic plaques to form.

The problem with this hypothesis is that LDL cannot get into any cell, let alone an endothelial cell, unless that cell wants it to. We know this, for certain, because the only way for LDL to enter any cell, is if the cell manufactures an LDL receptor – which locks onto, and then pulls the LDL molecule inside. There is no other passageway. This is an inarguable fact.

If LDL cannot enter a cell, unless allowed to do so, then it cannot pass through a cell, unless a cell wants it to. It most certainly cannot exit the other side of a cell, unless granted passage.

Others have argued that, oh well, the LDL simply slips through the gaps between endothelial cells and that is how it gets into the artery wall. Again, this is impossible. There are no gaps between endothelial cells. Endothelial cells are tightly bound to each other by strong protein bridges, known as ‘tight junctions.’

These tight junctions can prevent the passage of single ions – charged atoms – which makes it impossible for an LDL molecule to slip through, as it is many thousands of times bigger than an ion. This, too, is an inarguable fact. Ergo, the initiation of an atherosclerotic plaque (the underlying problem in cardiovascular disease) cannot be triggered by LDL leaking into an undamaged artery wall.

Which means that, if you want to get LDL (or anything else) into the artery wall, you first must damage the endothelium/lining of the artery. This has been accepted by the mainstream medical world, although you wouldn’t really know it, because they don’t exactly shout it from the rooftops.

Here, however, is a quote from the National Heart Lung and Blood Institute in the US. An organisation which is as mainstream as it gets:

Research suggests that coronary heart disease (CHD) starts when certain factors damage the inner layers of the coronary arteries. These factors include:

Smoking

High levels of certain fats and cholesterol in the blood

High blood pressure

High levels of sugar in the blood due to insulin resistance or diabetes

Blood vessel inflammation

Plaque might begin to build up where the arteries are damaged

It has taken them a long time to admit that damage must come first, but it is inescapable when you think about it. For once, I am completely in agreement with the mainstream on this, the initial step.

However, it is what happens next, where we rapidly diverge in our thinking. The mainstream believes that, after damage has occurred, it is LDL, and only LDL, leaking into the artery wall that triggers a whole series of downstream reactions that lead to plaques forming.

However, once you have damaged the endothelium there is no longer a barrier to stop anything getting into the artery wall. So, why pick on LDL? You also have proteins, red blood cells, platelets and Lp(a) and VLDL. Indeed, anything in the bloodstream now has free entry.

It particularly makes no sense to pick on LDL, as there is already plenty of LDL in the artery wall to start with. It gets there via the vasa vasorum (blood vessels of the blood vessels) which supply the largest blood vessels with all the nutrients they need, and through which LDL can freely flow into, and out of, the artery wall.

Which begs a further question. Why should the LDL that gets into the artery wall, from the blood flowing through the artery, cause a problem, when the LDL that is already there – does nothing? The more you look at it, the more ridiculous the LDL hypothesis becomes.

A counter hypothesis is as follows.

If you damage the endothelium, the first thing that happens is that a blood clot forms at that point. This has been known for a long time. I was sent an article a while ago, written as far back as 1959. The findings stand today:

‘…any intimal injury can very easily precipitate a local process of coagulation, platelet agglutination and fibrin deposition.’1 [a.k.a. a blood clot]

You may wonder where the word ‘intima’ just appeared from. The endothelium, and the thin layer underneath the endothelial cells is sometimes called the ‘intima.’ Sometimes it is called the endothelial layer, some people call it the epithelium, or the epithelial layer. What you never get, in medicine, is people calling it the same thing… the same damned thing. Thank God these people don’t make aeroplanes, is all I can say.

Anyway, damage the endothelium, and a blood clot will form. This is the main mechanism the body uses to stop itself from bleeding to death. Damage the artery/endothelium → underlying artery wall exposed → blood clot forms → life continues.

What then happens? Well, most of the blood clot is shaved down in size by plasmin, an enzyme designed to break up (lyse) blood clots. Then a new layer of endothelium grows over the top of the remaining blood clot, and in this way, the clot becomes incorporated into the artery wall. Although I have added in a few extra bits, this is, essentially, the thrombogenic theory, first suggested by Karl von Rokitansky in 1852.

He proposed this because he noted that atherosclerotic plaques looked very much like blood clots, in various stages of repair. He further observed they contained red blood cells, fibrin and platelets, which are the main constituents of a blood clot. His ideas were then rubbished by Rudolf Virchow, who could not see how a blood clot could end up underneath the endothelium, and Rokitansky’s theory (almost) died a death.

However, from time to time, other researchers also noted that plaques do look awfully like blood clots. For example, a researcher called Elspeth Smith – who taught me at Aberdeen University. She had this to say

‘…in apparently healthy human subjects there appears to be a significant amount of fibrin deposited within arteries, and this should give pause for thought about the possible relationship between clotting and atherosclerosis.’ 2

As her paper went on to say:

‘In 1852 Rokitansky discussed the “atheromatous process” and asked, “In what consists the nature of the disease?” He suggests “The deposit is an endogenous product derived from the blood, and for the most part from the fibrin of the arterial blood”. One hundred years later Duguid demonstrated fibrin within, and fibrin encrustation on fibrous plaques, and small fibrin deposits on the intima of apparently normal arteries. These observations have been amply confirmed but, regrettably, the emphasis on cholesterol and lipoproteins was so overwhelming that it was another 40 years before Duguid’s observations had a significant influence on epidemiological or intervention studies.’

Finally, for now, Dr Smith stated this in another paper:

‘After many years of neglect, the role of thrombosis in myocardial infarction is being reassessed. It is increasingly clear that all aspects of the haemostatic system are involved: not only in the acute occlusive event, but also in all stages of atherosclerotic plaque development from the initiation of atherogenesis to the expansion and growth of large plaques.’3

What she is saying here is that every step of CVD is due to various aspects of blood clotting. You damage the artery wall, a blood clot forms, it is then incorporated into the artery wall. A plaque starts, then grows. This description of how CVD starts and develops, is the process that I believe to be correct. With a couple of provisos.

The main proviso is that endothelial damage is going on all the time, in everyone’s arteries, to a greater or lesser extent. Therefore, we are not looking at an abnormality, or a disease, or a ‘diseased’ process.

The formation of blood clots following endothelial damage is also a healthy, normal, process. If it did not happen, then we would all bleed to death. As can happen in haemophilia, where blood clots do not form properly, due to a lack of clotting factors.

The next normal healthy process is that any blood clots that form must be incorporated into the artery wall. That is, after having been stabilised and shaved down. If clots simply broke off and travelled down the artery, they would get stuck when the artery narrows and cause strokes and heart attacks – and bowel infarctions and suchlike.

In short, the only way to repair any blood clot that forms on the lining of an artery wall, is to shave it down, then cover it over with a new layer of endothelial cells. Incorporating it into the artery wall.

At which point, repair systems swing into action. The main repair agents are white blood cells called macrophages. These break down and digest any remnant blood clot, before heading off to the nearest lymph gland where they too are broken down, with their contents, and removed from the body.

This ‘repair’ process leads to, what is referred to as ‘inflammation’ in the artery wall. Once again, however, this is not a disease process, it is all quite healthy and normal.

Problems only start to occur when the rate of damage, and resultant blood clot formation, outstrips the ability of the repair systems to clear up the mess.

Thus:

damage > repair = atherosclerosis/CVD

repair > damage = no atherosclerosis and/or reversal of plaques.

What factors can lead to the situation where damage outstrips repair? First, we need to look at those factors that increase the rate of damage. There are many, many, things that can do this. Here is a list. It is non-exhaustive, it is in no particular order, but it may give you some idea of the number of things that can cause CVD, by accelerating endothelial damage:

Smoking

Systemic Lupus Erythematosus

Use of oral steroids

Cushing’s disease

Kawasaki’s disease

Rheumatoid arthritis

High blood pressure

Omeprazole

Avastin

Thalidomide

Air pollution

Lead (the heavy metal)

Mercury

High blood sugar

Erythema nodosum

Rheumatoid arthritis

Low albumin

Acute physical stress

Acute mental stress

Chronic negative mental stress

Chronic Kidney Disease

Dehydration

Sickle cell disease

Malaria

Diabetes/high blood sugar level

Bacterial infections

Viral infections

Vitamin C deficiency

Vitamin B deficiency

High homocysteine level

Chronic kidney disease

Acute renal failure

Cocaine

Angiotensin II

Activation of the renin aldosterone angiotensin system (RAAS) etc.

Blimey, yes, that list was just off the top of my head, I could get you another fifty without much effort. And no, I did not just make it up. I have studied every single one of those factors, and many more, in exhaustive detail. The extent of how many factors there are, should not really come as a surprise to anyone, but it usually does.

After all, the bloodstream carries almost everything around the body, and the endothelium faces the bloodstream, it is the first point of contact. If damaging things are being carried about in the blood, the lining of the artery is going to be directly exposed to enemy attack.

Moving on, we need to look at factors that make the blood more likely to clot and/or make blood clots that are more difficult to shift. Again, in no particular order here and non-exhaustive:

Raised fibrinogen levels

High lipoprotein (a)

Antiphospholipid syndrome (Hughes’ syndrome)

Factor V Leiden

Raised plasminogen activator inhibitor 1 (PAI-1)

Raised blood sugar levels

High VLDL (triglycerides)

Dehydration

Stress hormones/cortisol

Non-steroidal anti-inflammatory drugs (NSAIDs)

Acute physical stress

Acute mental stress.

For good health, you want to maintain a balance between the blood being too ready to clot, and the blood not clotting when you need it to. If you turn down the blood clotting system, bleeding to death can be a problem. This can happen if you have haemophilia, or if you take warfarin – or any of the other drugs used to stop blood clots forming in Atrial Fibrillation. Aspirin can also lead to chronic blood loss, and anaemia.

Looking at it from the other angle. You do not want your blood to clot too rapidly, or else equally nasty problems can occur. Antiphospholipid syndrome (APS), is a condition where the blood is highly ready to clot (hyper-coagulable). It greatly increases the risk of CVD:

‘Patients with APS are at increased risk for accelerated atherosclerosis, myocardial infarction, stroke, and valvular heart disease. Vascular endothelial cell dysfunction mediated by antiphospholipid antibodies and subsequent complement system activation play a cardinal role in APS pathogenesis.’4

Just to look more closely at one other factor on the list, which is fibrinogen. This is a short strand of protein that is made in the liver. It floats about in the blood doing nothing very much. However, if a clot starts to form, or the clotting system is activated, fibrinogen ends up being stuck end-to-end to form a long thin, sticky protein strand called fibrin. This is a bit like the strands that make up a spider’s web.

Fibrin wraps around everything else in a blood clot and binds it all very tightly, creating a very tough plug. You would guess that if you have excess fibrinogen in the blood, more fibrin will form, creating bigger and more difficult to shift blood clots. I was first alerted to the dangers of having a high fibrinogen level by the Scottish Heart Health study.

‘This large population study confirms that plasma fibrinogen is not only a risk factor for coronary heart disease and stroke, but it is also raised with family history of premature heart disease and with personal history of hypertension, diabetes, and intermittent claudication.’ 5

To my surprise, a raised fibrinogen was found to be the most potent risk factor in the Scottish Heart Health Study, ranking above smoking. Because I don’t want to make this blog too long, I will simply say that all the other things in the list above both increase the tendency of the blood to clot and increase the risk of CVD.

Finally, we can look at factors that impair the repair systems. There are two basic parts to the repair systems.

Formation of a new layer of endothelium, to cover the blood clot

Clearing away of the debris left by the blood clot within the artery wall

What sort of things stop new endothelial cells being created?

Avastin

Age – which reduces endothelial progenitor cells (EPC) synthesis

Thalidomide

CKD – reduces EPC synthesis

Diabetes

Omeprazole

Activation of the renin-angiotensin aldosterone system (RAAS)

And drug that lowers nitric oxide synthesis

Lack of exercise.

What sort of things damage the clearance and repair within the artery wall?

Steroids

Age

Immunosuppressants

Chronic negative psychological stress

Certain anti-inflammatory drugs

Many/most anti-cancer drugs.

Knowing this, it seems counter intuitive that there has been a great deal of interest lately in using anti-inflammatory drugs to reduce the risk of CVD. My response to the idea that inflammation may cause CVD has always been that, the most potent anti-inflammatory agent known to man is cortisone/cortisol. This is one of the stress hormones, and it vastly increases the risk of CVD. As do immunosuppressants – which are also used to dampen down the inflammatory response.

On the other hand, inflammation is not always a healthy thing. There are many chronic inflammatory conditions such as: rheumatoid arthritis, Crohn’s disease, asthma, Sjogren’s disease and suchlike where the bodies immune system goes wrong and starts to see proteins within the body as ‘alien’ and attacks them. This can cause terrible damage.

The way to best treat (if not cure) these conditions is to use immunosuppressant drugs. Cortisol/cortisone – and the many pharmaceutical variants that have been synthesized from cortisol – is still widely used. Hydrocortisone cream, for example, is widely used in eczema.

Immunosuppressants are also commonly used in transplant patients, to stop the organ from being attacked by the host immune system. This is a good thing to achieve, but longer-term problems with CVD are now widely recognised.

‘With current early transplant patient and allograft survivals nearly optimized, long-term medical complications have become a significant focus for potential improvement in patient outcomes. Cardiovascular disease and associated risk factors have been shown in renal transplant patients to be related to the pharmacologic immunosuppression employed.’6

‘Taking high doses of steroids (glucocorticoids) seems to increase the risk of heart disease including heart attack, heart failure, and stroke, according to new research. Steroids fight inflammation and are often prescribed for conditions including asthma, inflammatory bowel disease, and inflammatory arthritis. Prednisone and hydrocortisone are two examples of steroids.

The question I suppose is, can CVD possibly be a form of autoimmune condition? It seems highly unlikely. Although the inflammatory system can go wrong in all sorts of way. You may have heard of Keloid scars. These happen when you damage the skin, and the resulting healing response can create a very large ‘hypertrophic’ and unsightly scar.

Perhaps if you damaged the lining of an artery, and this triggered the equivalent of a ‘keloid’ scar in the artery wall, then if you could dampen down this reaction, an atherosclerotic plaque would then be much smaller. In which case, an inflammatory could be of benefit.

However, as of today, the more potent the anti-inflammatory drug, the greater the increase in CVD. Which suggests that if you interfere with the healing response to arterial injury, you are going to make thing worse – not better.

In truth, the real reason why inflammation is being seen as a possible cause of CVD is because inflammatory markers can be raised in CVD. To my mind this just demonstrates that in people with CVD, lots of damage is occurring, therefore there is more repair going on, so the inflammatory markers are raised.

However, the mainstream has decided to look at this from the opposite side. They see a lot inflammation going on and have decreed that the inflammation is causing the CVD – rather than the other way around. Frankly, I think this is bonkers. But there you go.

Anyway, where has all this got us to. I shall try to achieve a quick summary.

The LDL hypothesis is nonsense, it is wrong, and it does not remotely fit with any other factors known to cause CVD.

The thrombogenic theory, on the other hand, fits with almost everything known about CVD. It states that there are three, interrelated, processes that increase the risk of CVD:

Increased rate of damage to the endothelial layer

Formation of a bigger or more difficult to remove blood clot at that point

Impaired repair/removal of remnant blood clot.

Any factor that does one of these three things can increase the risk of CVD. Although, in most cases, a few factors probably need to work in unison to overcome the body’s ability to heal itself. Which means that people who have only one or two risk factors, are probably not going to be at any greatly increased risk. You need to have three or four, maybe more, and then things really get going.

There are a few things that I have mentioned that will greatly increase the risk of CVD with no need for anything else to be present. They are:

Steroids/Cushing’s disease

Chronic Kidney Disease

Sickle cell disease

Antiphospholipid syndrome

Immunosuppressants

Avastin

Diabetes

Systemic Lupus Erythematosus

Kawasaki’s disease.

All of which means that – in most cases – CVD has no single, specific, cause. It should, instead, be seen as a process whereby damage exceeds repair, causing plaques to start developing, and grow – with a final, fatal, blood clot causing the terminal event. The next blog will be a review of the things that you can do to reduce your risk of CVD.

318 thoughts on “What causes heart disease – part 59”

I have a web site where I’ve saved all of these “parts” if people want to read them starting from Part 1, up and through this one! If anyone wants to do so, just say the word and I will post the link to my site.

You can also read the archives. Start with https://drmalcolmkendrick.org/2016/01/ (January 2016 = first three posts) and work your way forward, month by month and year by year, by changing the date in the url.

I agree! Amazon is just as bad as most personal physicians who insist on having you take blood tests for lipids, when in fact a lot of us don’t believe any of that is important enough to worry about and most of us also don’t want to pay for it. It astounds me that insurance will pay for cholesterol blood tests but they refuse to pay for Vitamin D3 level testing.

Does anyone have an easy way to convince a personal physician that we wish to have higher cholesterol numbers as we age, not lower numbers?? I have tried and tried to tell my dr that, but it goes in one ear and straight out the other.

And I am now so confused about the blood pressure issue that I’ve completely given up trying to figure it out.

I’ve had this in the past, and when it happens I usually can’t post on many or any blogs, including ones owned and run by friends. Either something I do offends the Gods Of The Internet or someone actively blocks me. After a while whatever it is wears off. Sorry it has also happened to you but a relief to know I’m not the only one.

Among my theories – if you post too many replies too too many blogs, or especially replies with links, you trigger a spam filter. Akismet claim it is not them but of course they would say that if they thought I was a spammer . . .

Thank you, I was trying to remember that quote and who said it. A friend used to use the term “ficts” for things that sounded logical but were completely wrong. Lots of ficts in medicine, mostly repeated by The Anointed and their organisations. Lots of facts too but you don’t get told about them, you have to dig them up for yourself or find them on blogs such as this, or Twitter.

Hi blood pressure is more of a symptom of CVD than a cause is it not ? And cholestoral is not really a cause either, if u have been following the postings here u might hav concluded. I developed CVD with no history in my family. (Could it be the family’s lifestyle passed on from generation to generation?)

Thanks Dr.Kendrick for another superb breakdown of the real and clearly multiple causes of CVD. I am tempted to side with Private Frazer and conclude that “we are all doomed” but given that we all have to die of something , I await eagerly your next blog indicating how we might at least delay the “remorseful day”.Keep up the great work and look forward to your next book. John d

Jean, when Dr. K first started this series, I was printing them, as well. But when I could see there were going to be lots more parts upcoming, I decided to save them to my forum and not try to use up all the trees around me!

One thing I now wonder about is the connection between food and the suppression of our immune system. It is known that vegetable oils rich in omega 6 were early used to supress and improved the outcome of the kidney transplants. As far as I remember sunflower oil was preferred with good results. However this practice had to be abandoned since the patients were getting cancer at an alarming rate.

This now begs the question about an additional connection with CVD. I something known about this scientifically? In my own case I strongly suspect such a link and today I stay away from all these polyunsaturated oils.

I would love to see a simple graph on heart disease and the use of industrial seed oils as food. It seems to me like it is just as likely that they would correlate as anything else since they began to be used in the early 2oth century, about the same time heart disease began to rise. Any data?

Mia: A group at the University of North Carolina dug out one of Ancel Keys’ studies which he had never published, likely because it contradicted his life’s work. I can’t remember the name of the researcher, but he is a credible researcher who also works for the NIH. Eatthopology (Adele Hite) probably has more information about this.

One of the issues with high-PUFA oils is they look good on paper. If you feed humans a high-PUFA keto diet and compare with a high saturated fat diet, their blood sugar and insulin come down, leading to increased insulin sensitivity. Looks great on paper. But if Hyperlipid and Eades are correct, what’s happening is the PUFAs cause fat cells to be insulin sensitive, meaning they take in more insulin and consequently more blood sugar. Ostensibly, you’re getting more “insulin sensitive”, because you’re getting fatter.

Mike. I have read Ray Peat in the past. I still do not think there is sufficient clarification made between consumption of plant oils and consumption of the whole seed/nut. He does actually mention that whole foods, when fed to cattle and pigs, produces meat which is detrimental to human consumption. But can we extrapolate that to mean that when whole seeds/nuts are consumed by humans, it is as bad for us as using the oil alone pressed from them?
I can see the sense of eating meat and dairy products derived from grass fed creatures, but where can that be obtained from with relative ease, let alone within the pockets of the majority?

Mike Paul, thank you for that link. It’s just increased my stress (oxidative I expect) level when I see bacon is appears as bad as.taking the oil itself. From the link:

“Linoleic and linolenic acids, the “essential fatty acids,” and other polyunsaturated fatty acids, which are now fed to pigs to fatten them, in the form of corn and soy beans, cause the animals’ fat to be chemically equivalent to vegetable oil. In the late 1940s, chemical toxins were used to suppress the thyroid function of pigs, to make them get fatter while consuming less food. When that was found to be carcinogenic, it was then found that corn and soy beans had the same antithyroid effect, causing the animals to be fattened at low cost. The animals’ fat becomes chemically similar to the fats in their food, causing it to be equally toxic, and equally fattening.

We keep seeing we need to consume lino products (also used for floor coverings at one time I think) but even if we try to eat saturated fats, the manipulators have got there first. It is now illegal in the UK to feed pigs the swill they once ate because of the false claims of foot and mouth disease links (Lots available on warmwell.com) so they are now fed on inappropriate crap.

Ah, I would take what Ray Peat says with a degree of caution. According to Chris Kresser:

“On average, grass-fed beef tends to have slightly lower levels of MUFA and slightly higher levels of PUFA than grain-fed, but these differences are at most five percentage points, depending on the breed of cattle and the study in question. So regardless of whether your beef is grain-fed or grass-fed, you’ll be getting about 40-50% saturated fat, about 40-50% monounsaturated fat, and somewhere near 10% polyunsaturated fat… What you’ll be missing out on are the significantly higher levels of omega-3s found in grass-fed beef.” — https://chriskresser.com/why-grass-fed-trumps-grain-fed/

Sunflower oil is about 60% polyunsaturated fat, so beef fat is nowhere near “chemically equivalent to vegetable oil.”

Goran. Do you avoid the polyunsaturated oils even in their natural state? I never use the extracted oils as such, ( which is what I think you are referring to), no matter how they are produced, as I regard them as processed products. However, I eat quantities of the whole, raw foods which are rich in them, as I understand they are essential for good health, and the only way our body can access them. I hope I am being sensible about this subject, as I have read round it for many years now, and have concluded that all nuts and seeds are healthy.

Jennifer surely that depends on which unprocessed oil you mean. Sunflower seeds were domesticated in Northern Mexico/SW USA by the native Indian community tribes there..And have been part of the diet for centuries. On the other hand Canola oil comes from the slightly modified Rape seed plant ( a brassica species) which was never eaten by humans but only grown as a crop for feeding to livestock..It was never eaten by humans because it is poisonous for humans…I suspect that Canola, despite the breeding done, still has the poison in it. Another polyunsaturated oil is Palm oil..It is native to West Africa. Again this is a very recent addition to the diet of humans. And the raw palm oil nuts are not very edible. It was originally used to make soap by Lever & Kitchen.. So again I am suspicious.

Bill in Oz: According to “Know Your Fats,” rapeseed oil “. . .has been very popular in India and China for centuries.” So erucic acid may not be as toxic as we have been led to believe. She also says that “Erucic acid has been used as a specialty fatty acid for treatment of leukodystrophies.” Only Dr. Kendrick would know what that is!

Jennifer: Absolutely right. Essential Fatty Acids (EFA’s) are called that because they are dietary essentials. Our bodies need them, but cannot produce them. The two we need are the omega 3 and omega 6 (called this to designate the position of the first double bond relative to the omega end of the fatty acid, as opposed to the carboxyl end). There are two main problems with industrial seed oils: 1. They may be rancid when used; and 2. They have a very high omega6/omega3 ratio, which is not healthful, especially considering the large amounts of them many people eat (most processed foods and restaurant foods contain them, as they are cheap). Nuts, too contain a high 6/3 ratio, but we don’t eat very many of them, and they are jam-packed with nutrients, especially minerals. I eat some every day. We can solve the problem of the 6/3 ratio by eating seafood. Fresh, frozen, smoked, tinned. All good.

No Gary, that is misinformation.Mustard oil has been popular for centuries in India..Another brassica yes..But it is not the same as Rape seed oil which was ‘bred’ in Canada in the 1940’s as a ‘break crop’ from wheat…And it is used for that purpose still…

Bill in Oz: I stand corrected. The information came from Dr. Mary Enig’s “Know Your Fats.” By the way, Canadians can be very sensitive about this issue. I like my Canadian friends very much, but I never mention Canola oil or tar sands in their presence.

As Bill points out we need both the omega3 and the omega6 and both in limited amounts – a few grams per day and roughly in equal 1:1 proportions. The problem of todays nutrition is the we are “drowned” in the omega 6 and the omega 3 is scarce. As far as I remember there was liberal quantities of omega 6 rich sunflower oil administered to the transplant patients before they had their transplanted kidney with the explicit purpose to surpress immune reactions.

Once I dug deep (the “thick” books!) into the fat/oil chemistry (my favorite subject) of our food and the metabolism involved but very soon became quite overwhelmed by the complexity as I have also become with most metabolic processes in our bodies. (This post excellently discloses this complexity for the CVD issue.) It is in my eyes thus important to avoid categorical statements but still, out of caution, I stay away from all those vegetable oils (except virgin olive oil) wether processed or not.

BTW Coconut oil is a special vegetable oil since it is mostly a saturated fat and in my eyes one of the most healthy fats you can digest since it is a short chain fat that readily metabolizes in the liver to produce ketons which is the superfuel in our bodies, e.g. your brain loves it.

Thank you for the summary. In October, while on vacation, I read through most of the “What Causes Heart Disease” series. Great stuff and very helpful to a CABGx4 survivor. I recently stopped taking pantoprazole after reading your blog.

An excellent summary Dr K. It got me thinking…sometimes I wish I was blissfully unaware about some of the factors. For example I found out many years ago I was heterozygous for Factor V Leiden. I think the more the more you find out, the more you stress – and you know what stress does. Perhaps all these ‘diseases’ such as high blood pressure and cholesterol are causing us to stress too much about risks that quite frankly are too low to worry about.

Several environmental and health organizations and individual mothers on behalf of their children are suing EPA in Federal Court in the US to ban fluoridation based on neurotoxicity. The case is moving forward and is scheduled to be heard August 2019 despite EPAs attempts to get it dismissed and to limit discovery.

I just finished reading a book about Reversing Heart Disease by Dr. Daniel Cobb, DOM. It’s fantastic! He uses Pauling Therapy with a few additions with great success. He gives specific supplements and dosages if you want to do it yourself. You can download it for free here: http://www.danielcobbdom.com

Tell me, how much Vitamin C does Dr. Cobb recommend we take on a daily basis. I don’t know about you, but I start getting loose bowels at 500 Mg or even less if taken all at once. And usually these Pauling disciples recommend far more than that.

I emailed Dr. Cobb, he said there was a web host problem which is fixed now, and should be functioning by tomorrow. The book is really outstanding!

I too find taking a lot of vit. C is tough on my intestines. Dr. Cobb says “For someone who is an advanced heart disease patient, I usually recommend somewhere between 6 and 12 grams/day. For someone who merely wants to take this formula as a preventative, I recommend about 3 grams/day.”

I’ve started trying some different liposomal C products, which are very easy on the intestines and have much higher cellular absorption rates. 1 gram of liposomal C = 6 grams regular C. I wanted a product that is free of soy, chemical preservatives, and sugar/glycerine. The only one I found that met these criteria is from Lipo Naturals, which I just started today – so far feels very good.

See http://qualityliposomalc.com/
Dr. Levy has financial ties to LivOn. Homemade Liposomal C can be made as good or better than the commercial products such as LivOn according to the highly experienced author of that site.

AH Notepad
about Aluminium adjuvants in vaccines. Aluminium is the most common element in the earths crust, and is present in many vegetable, potatoes spinach etc. We consume, I think 8 to 10 g a day. If this is so, will a bit extra in a flu vaccine harm me?
I am pleased that you have never had flu. I have had it badly twice in my life, I take the vaccine to avoid a third go

Mr Chris, I will have to bow to your knowledge about aluminium consumption in diet, though it seems a large amount. The amount of aluminium in vaccines is 850 micrograms. The safe dose extrapolated from vaccines for infants for an adult weing 80kg would be 400micrograms per day. I doubt it is acceptable to just double the figure and say it is not given very often so it will be ok. Aluminium ingested through diet has a mechanism which will excrete it reasonably quickly particularly if you are 1) taking sufficient vitamin C (or other suitable antioxidant) 2) if you are consuming sufficient water containing >30mg/litre of silicates (Ref Chris Exely)
.
Injected aluminium, or any thing else for that matter does not have a protective mechanism to deal with it,https://thinklovehealthy.com/2017/06/22/aluminum-in-vaccines-history-and-toxicity/

AH Notepad,
sorry there was a typo in my reply, daily consumption is 7-9 mg per day!
Now you are right about the difference between adjuvants and dietary aluminium, the truth is I don’t know how the body handles it.
My own thoughts are that if its a toss-up between flu and aluminium adjuvants, I would prefer to not have flu.

Mr Chris, I would prefer not to have flu, I would prefer even more not to have what is largely an ineffective vaccine, which has some effects listed https://www.medicines.org.uk/emc/files/pil.666.pdf which are an indication of a system hyperstimulated into reacting to substances we were never built to deal with, and merely to provide a response where antibodies to the vacine can be detected, yet this indication does not translate to immunity. I note the leaflet doesn’t tell you all of the ingredients or how much.

I can deal with the possibility of getting flu, by maintaining a system that isn’t likely to be attractive to a flu virus. https://youtu.be/LSgNiBgN2Hk

Mr Chris: Read what Professor Chris Exley has to say about aluminum adjuvants (simply search by his name; he is the world’s foremost authority on the biological effects of Al). Yes, we all carry an Al burden, through ingestion. It is an entirely different matter for the body to deal with Al, or anything else, injected into muscle tissue. By the way, none of the influenza vaccines (at least those licensed in the U.S.), contain Al salts. The majority of vaccine injuries compensated in the U.S. under the National Childhood Vaccine Injury Act of 1986 are for adults for injuries from the flu vaccine, many of them for a diagnosis of Guillan Barre (which involves paralysis).

Really? I would be interested as to why nutrition won’t work. It works for almost all other diseases, certainly better than the toxins offered by the medication industry. The main problem nowadays is nutrition might be ineffective is the nutrients available from food is so woefully low compared to that available before industrial agriculture.

Nutrition won’t keep you from dying. I’m supposed to believe that all those people who died over the decades did so because they were drinking Big Gulps? Note this doctor also thinks that AIDS is caused by eating the wrong foods. Amazing that gay men eat badly and non-gay men eat correctly.

Virtually the only non-gay men who get AIDS are ones who share needles while shooting drugs with others or closeted ones who have gay sex. True transmission of HIV from female to male by sex is almost non’-existent.

Chris C – I question the accuracy of HIV/AIDS reporting in Africa. You have massive areas of poverty where they have no sanitary water and people have barely enough to eat, and somehow international organizations are able to produce percentages of people who have HIV that we are supposed to believe are accurate. Many times people are just assumed to have died of AIDS even if no blood tests were done on those people. And we do not know what the private lives of many of the people are. But even these reports indicate that HIV is much more prevalent among women than men.

Mark, in South Africa most pregnant African women will go to a government clinic for their checkups, even in deep rural areas. They will automatically be tested for HIV so they can be given the appropriate medication to prevent mother to child transmission during birth if necessary.

The rate of HIV infection can be up to 35% among pregnant women in some areas. The total burden of infection in the whole population is extrapolated from clinic figures using internationally accepted formulas.

Drug use would mostly be by smoking, like marijuana or nyaope (a home-made concoction of marijuana, heroin, rat poison and anti-retrovirals, allegedly), or white pipe in my area (marijuana and Mandrax). There is little needle sharing AFAIK.

While there is a low risk for a man to get infected from an HIV-positive woman in any one sexual encounter, obviously if you have a lot of sex the chance of getting infected goes up proportionately, and in poorer areas there’s not much else to do, plus women will exchange sex for food. Also, uncircumcised men are more prone to infection (circumcision is common in some tribes but not in others), and there is also ‘dry sex’ where women dry out their vaginas with herbs, which enhances the pleasure for the man, apparently (never tried it myself), but leads to increased micro-tears of the vaginal wall and hence chance of infection.

What is “the test for HIV”? Is it a test for antibodies? If it is what does that prove? Test most of us for measles, chicken pox and a few other diseases, we’ve probably got them. This medication business smells a bit. A bit like finding the “cure” for cancer.

Thank heavens for the test. Before the test, you ran the risk of getting AIDS from blood transfusions, as many did who were not gay or intravenous drug users. Now infected blood can be detected and eliminated from the pool.

The test can also determine if you need ARVs. Of course, you could always refuse to take them if you don’t believe they do any good. But please don’t deny others the opportunity to take them. Back when our president was a fan of Duesberg’s theories, hundreds of thousands of infected people who could not afford ARVs didn’t get state-purchased medication, and died early deaths from AIDS.

Fortunately the authorities saw the light and HIV testing and ARVs are now available from government clinics. People are still getting infected at the rate of about 1,000 a day, but it’s not escalating like before.

Great summary. Though where are the knowledgable counter-arguers these days? Is it my imagination or is there less heated debate on this blog lately? Not that I’m personally missing it particularly I must say. Hoping things are quieter because the soundness of your position is unassailable, Dr.K.

I was about to simply chirp ‘Absolutely’ in reply – I doubt many of us want to live in scientific totalitarianism and it has been much to your credit imho that you’ve always emphasised the need to be open to falsification for good science to happen and allowed disagreeing voices in the blog comments even if it inevitably gets messy sometimes – though I then hesitated slightly as of course nothing is ever quite that simple and, perhaps a bit pedantically, and perhaps unnecessarily stating the bleeding obvious, I don’t think that it is strictly the only way ideas or science progress / get improved. Sometimes ideas are delicate new creatures that need protecting and shouldn’t be trampled to death immediately, we also develop our ideas ourselves or by bouncing off others, and a blog forum that is just a big bunfight (even if a ‘scientific’ one) is probably not much help, or fun, either… In the end though, it is negative feedback that is the key systems control principle.

Happily the admirable community frequenting this blog forum seems to provide almost entirely considerate, constructive and supportive input! Or are you doing much more filtering than we are aware 🙂

This is extremely helpful to me, thanks very much! I recently wrote about blood clots and Celiac Disease because several people have already written (before me) that they had a clotting event either before or soon after they were diagnosed with CD. I also had an unexplained clotting event and later found out I have CD. But it doesn’t seem like the two are officially connected, other than CVD is an associated illness with CD. I’m guessing the connection is that CD is an autoimmune illness, but people don’t get immune suppressants for it, unless it’s ‘refractory’ (not solved by simple means, that is, the gluten free diet).

Many of the risk factors you mentioned were mentioned over and over in the articles I found on clotting in CD, the one that stands out is antiphospholipid syndrome. I’m just an amateur, but I remember enough biology to know that that would be horrible for endothelial (and any other) cells. It’s bizarre to me that the body would ever form such a condition. It’s like a suicide pill. Do we know what the cause of APS is? I mean, what causes the body to go so fundamentally off course?

I have a question about NSAIDs, do they cause the formation of harder to remove clots? Because I’m pretty sure they are universally thought of as blood thinners. For instance, I stayed away from ibuprofen during menses because it would cause a horrendous heavy flow. But it was the best for pain control, so it was always one of those catch 22 drugs in my mind. And aspirin is used supposedly to prevent blood clots. Also, I now take huge doses of Vitamin E during menses because while they increase flow, it’s not as much, and it stops pain just as effectively as ibuprofen (for me).

I didn’t know about several things you mentioned, for instance, fascinating that the artery wall has its own blood supply! I’d love to see a list of “these things can help reduce fibrinogen levels, or otherwise help repair the artery walls better.” I can guess at a few, Vitamin C, and others, not smoking, taking gentle chelation agents like chlorella to keep too much heavy metals from hanging around the body for too long… but I’d love to see some supportive care ideas.

I love the idea that inflammation has a purpose, because there are athletic articles that come to that very same conclusion.. ie. that you get better muscle and tendon repair if you do NOT take NSAIDs after workout. There’s a limit though… acute mental anguish can result from too much physical pain. As someone who has suffered pain since toddlerhood, I can testify to that.

Some alternative thinkers believe that autoimmune problems are actually caused by microbes. Either an ongoing infection or a past one. I suppose an example would be strep throat –> scarlet fever –> heart damage. An angle that gets overlooked is fungal infection. According to Doug Kauffman, one of the big mainstream outfits recently said that most sinus infections for which people are given useless antibiotics are actually fungal, so they should take an antifungal.
His book I found most interesting on this topic is called Infectious Diabetes.
I find a lot of merit in this approach. It makes sense to think if a very intelligent system goes mad that there was a cause. As time goes on I think more and more incorrigible and mysterious conditions will turn out to have a viral or fungal root cause. I think cancer will also succumb to this.
Bacteria also, but perhaps less so as we know more about them.
There are general blood tonics which are fairly harmless and might make a big difference to a lot of people’s health, such as ingestion of pure turpentine and colloidal silver. But I recently read that colloidal silver is not legally sold in the EU!
Is this so? Well, one can buy a generator and make it oneself.
Other blood tonics include ginger, garlic and oregano oil, and others. But the garlic and ginger need to be raw.

Hannah Yoseph MD wrote, How Statin Drugs Really Lower Cholesterol and Kill You One Cell At A Time which explains how statins work on a cellular level and also tells the sordid history of how they gained FDA approval.

She’s also written several books on the fungal causes of autoimmunity. Here’s one on cancer which is very interesting because statin drugs are fungal toxins and statins and their original use was in cancer research. Cancer patients have low blood serum cholesterol because cancer cells take up lots of cholesterol.

AnnaM: Don’t forget vaccines. Yehuda Shoefeld, M.D., the world’s leading auto-immunologist, co-wrote and edited a medical textbook, published in 2015, on this very subject. I believe the process is molecular mimicry, that is, vaccines can contain foreign proteins which are similar enough to human proteins that can trick the immune system into attacking its own tissue. They are produced using human fetal, dog, monkey, and other animal cells, and chicken eggs. Nobody knows all the ingredients in any vaccine, and they are mostly injected directly into muscle tissue, bypassing the normal route for invading pathogens. By the way, thanks for the information. I take raw ginger and garlic every day, and feast on garden oregano from time to time.

Gary, it may be over-stimulation of the immune system that causes self-attack, without the need for foreign proteins. The components causing the problem are the adjuvants which is a very unnatural substance to have in the body. Still, nobody has done any studies on adjuvants, or at least studies where the data showed they were safe enough to publish the figures.

AhNotepad: Yes, adjuvants are a great concern, another piece of the puzzle of how vaccination harms so many, while providing little, if any benefit. In my view, it is a completely failed paradigm, like the cholesterol theory of heart disease. One example: Varicella vaccine is mandated (since the mid-’90’s) in the U.S., but not in the U.K., for the very sensible reason that chicken pox is a mild childhood disease, and the vaccine has led to a rise in shingles in adults, and, unheard of before the vaccine, in children. More trouble than it is worth. That’s the official word from the U.K. health authorities. But they will never take it off in the U.S. They never take them off, except to replace them with a more expensive one.

My 15 month old grandaughter aquired chicken pox recently, from distress to recovery was about 5 days, with only two of them bad. But then she doesn’t get vaccinated, at all, and she gets loads of sodium ascorbate. My son then got it, three days rough, and then a couple of days recovery, but then he was taking about 5 grams of liposomal C every day, and loads of sodium ascorbate. It works!

Mr Chris, I have been with my wife for over 40 years, in that time we only contracted something that could be termed flu, once. Neither of us has ever had one of those aluminium, formaldehyde, egg+human+monkey cell+virus concoctions (plus all the other foreign substances) ephemistically described as giving protection against something or other. We don’t know whether it was flu, as nobody who gets something like that, ever gets an analysis to determine the pathogen. However we haven’t had our immune systems hyper-stimulated with aluminium and so have a lower risk of degenerative brain disorders and auto immune diseases than someone who has. I now get loads of immune system support from sufficient doses of vitamin C.

Wow this is a really great discussion. Let me add to the ideas by mentioning a triple board certified American MD, Zack Bush, who has been interviewed several times by “health hacker” types on youtube. If he’s crazy, then he’s crazy like a fox, because he could’ve given this speech (below) at my college and fit right in with my education in Environmental Science. To grasp some of his ideas you have to know how glyphosate is patented, so you might want to search this page for ‘patent’ before watching: https://gmofreeusa.org/research/glyphosate/glyphosate-overview/

There are several others, the famous interview he gave was with the Bulletproof Executive, but I think this one is more recent. His premise is convincing to me, and has to do with regaining our balance with the natural world, especially microbes. He’s part of the growing interest in the human flora and how it can be recovered after it has been damaged.

I think he would agree with some of the anti-vax ideas proposed by others, but I don’t know for sure how he feels on that subject, he’s just mentioned it a few times. There’s plenty to criticize about vaccination, and plenty to consider such as, I’m not going to claim that the Black Death was a good thing, or smallpox or anything else that kills people and those are obviously pathogens. Also, if the Celiac vaccine works, then it would be the first time that a vaccine stopped an autoimmune process, so how does that fit the theory (that vaccines cause autoimmune)?

What I’m saying is, this is a deep subject and for now I’m taking an open minded and not decided view on it.

Angelica: It is indeed a deep subject. There are an enormous number of resources available for the education of the public. All good science. The entire media denies that anything is amiss, and ridicules and defames anyone who raises questions about vaccine policy, regardless of the scientific merit, regardless of the shocking state of children’s health, not just in the U.S., U.K., and Ireland, but all over the world. So you cannot trust anything on this subject in the media. They are financially conflicted, and ignorant in general about scientific issues. So the truth of the matter is likely to be the opposite of what they say. I have read a great deal of this science, of the history of vaccination, and heard hundreds of stories by parents, in person, in interviews, and in blog posts, concerning serious, life-threatening reactions to, particularly multiple, vaccinations. I know enough now to state, without question, my belief that vaccination is 18th Century quackery. Our vaccine injury compensation program here in the U.S. has just passed $4 billion paid since FY 1988. Only a tiny percentage of such injuries even make it to this (administrative proceeding; there is no legal recourse), and only about 1/3 actually win compensation. Vaccine policy is a cesspool of corruption.

Gary,
Vaccination is a very interesting and contentious topic . . . and not on point here.
Weren’t you and Malcolm going to put together a dedicated vaccine blog where the presentation and comments (and counter comments) can be exhaustive . . . and on point?

JDPatten: It probably won’t happen, which is fine because there are many resources available on line. The striking parallel between the mainstream heart disease model and the mainstream infectious disease model is that both are wrong, and both are so tangled up in financial conflicts and have become so lucrative that change will only come from public awareness and demand. What is frightening is governments mandating medical treatment of the healthy which has little value, and is dangerous for some. Education, and a true risk/benefit analysis is important for public policy, and choice, in terms of medical treatment, especially of the healthy, essential in a free society.

Yeah I guess that discussion did go off course a bit. My question is still there though. Anyone know if certain NSAIDS cause clots and others thin blood? Because I’m pretty sure aspirin opposes blood clotting, and so does ibuprofen, but I’m not sure of the others. The mention of NSAIDS causing more blood clotting surprised me.

A statin is designed to deal with the LDL/cholesterol hypothesis. What is the statin doing if in fact the Thrombogenic theory is correct? If calcium deposits are part of the repair system and statins increase the calcium that is deposited. Does that mean a statin is helping the repair system and lowering the volume of unstable plaque?

Thanks for all your work Dr. K, we need more people like you working on this conundrum. So that’s why a statin is prescribed as a preventative measure………. as a Nitric oxide enhancement strategy and protection against clots? But they also seem to have a role in repair, for many people their CAC score goes up after taking statins. I have been in contact with a man that has a 4400 CAC score………….. he has been taking statins for over 20 years. In this case is a high CAC score protective?

A friend of mine was recently put on a statin by his cardiologist because he had an elevated CAC score. I pointed out to him that there is research that shows that statins actually accelerate the process of calcification. He raised this with his cardiologist ( a professor no less) who said that this was a good thing because it helped stabilise the plaque.

I really do struggle with the proposition that “some” calcification is bad because it increases your risk of CVD, while “more” calcification is good because it lowers your risk of CVD.

If this proposition became generally accepted then the drug companies could achieve their aim of statinating the entire population.

Another nitric oxide enhancer is the “nitric oxide release workout” or “nitric oxide dump” – a four-minute high intensity exercise programme, to be repeated several times a day. Probably great as a preventative measure (with the nice side effect of providing you with a firm behind), but maybe less suitable for the already frail/sick.

This fits with what I learned about statin use in the elderly after a stroke. My family decided to leave the statin my father in law is taking on his list of meds (we did a health restart for him and my mil) because the science showed it prevents another stroke, but only of certain types of strokes (his type). If it’s just anti-coagulation, then wouldn’t it be unnecessary since he’s on warfarin anyway? A person doesn’t know which way to jump. I guess we an only do our best in the circumstances.

Jim, I joined this blog almost at the start because the topic was about statins, if my memory serves me correctly. I had read Dr Kendrick’s book, the Great Cholesteral Con, and mentioned it to my GP when it was 1st published, and it was po-pooed, so I binned the book, and continued taking the stains for several more years. Within time, my medication list was so long. As I was approaching 65 years of age, I decided to buy the book again , then plucked up the courage to seek advice yet again from my GP, as my general health had declined to a serious state. The rest is history, as I was again given short shrift, only by then I felt more empowered having read round the enormous topics of Big Pharma and the problems of industrialised food production, and the fascinating subject of fats.
So, if you can find a way to access the early blogs, I am sure you will enjoy them.

The “statins are good because they stabilize plaque theory” is in response to the studies indicating statins increased plaque formation. This way, statins are still “good”.

I saw a twitter fight about this very subject. The statinators were pointing to studies where the “density” of the plaque was “better” for people taking statins. Whether this is good or bad, to me, remains an open question. Maybe thicker but less dense is better? Or maybe thinner but more dense is better?

Thanks again Malcolm. What I really appreciate is that you write so we will understand – clearly and simply with the odd ( needed ) nugget of humor.
If only more medical ‘scientists’ or ‘doctors’ could think this through so well.

Great summary of your thinking Malcolm . I like the notion of a fault in the normal balance of ongoing repair/damage in the artery . It fits with the way so much physiology is a constant homeostasis and feedback loopdand where illness can occur with imbalance of these .

It says that NO production from L-arginine depends on nitric oxide synthase (NOS) enzymes. However, the paper claims that ” since most chronic diseases are characterized, or at least associated with dysfunctional NOS, NOS-dependent strategies utilizing L-arginine and/or L-citrulline have proven largely ineffective.” In support of that statement the paper gives links to 2 studies of L-arginine supplementation: one in PAD and another following MI. According to the author, both failed to show benefit.

Thus, the paper claims that strategies to enhance NO availability that rely on co-factor or substrate supplementation (L-arginine, L-citrulline, ascorbic acid, folic acid, tetrahydrobiopterin BH4) all require functional NOS system which is apparently faulty in chronic illnesses.

I was wondering if anyone more knowledgeable on here can comment on how NOS enzymes figure into these supplementation protocols and whether people who supplement with any of the above notice subjective improvements in their well-being and specifically in health issues related to NO production.

Sasha: Thank you for your question. I would assume we produce sufficient NOS in the normal course of things, but don’t really know. I’ve been taking L-arginine/L-citrulline only on my workout days, and only for a few weeks. In general my workouts have been going better over the past few months, and the only thing I’ve changed in that time is the Al-reducing protocol. I’m sleeping 8 hours now most nights, after sleeping only 7, sometimes 6, for years. I also seem to be a bit more cold-tolerant. We shall see what discussion ensues on this interesting question!

Thanks Gary, for your response. I am very interested in that question. The author has a stated conflict of interest because he co-founded a company that produces a supplement that contains beetroot and hawthorn but apparently that supplement has been clinically studied in University of Texas. He also co-wrote a book on all things NO. I would like to read it but it’s about 100 bucks on Amazon…

Sasha: Bill in Oz knows more about this than I. I simply picked up what our local health-food store carries. They have more than one brand, but I got Jarrow Formulas. Pretty pricey. If I used it every day, it would run $2-$3 per day.

About beetroot: Fermenting them breaks down the sugar, so that should be a safe option. I started a new batch of fermented beetroot the other day. It’s very easy to do and it tastes nice. Better than kimchi. I can share my recipe if anyone is interested. I avoid beetroot juice since I fear it will cause a spike in blood sugar. However, there’s lots of fiber in beetroot so I figure eating them whole or having them in a smoothie could be ok. A low-sugar alternative to beetroot is rucola.

Thank you, such a useful drawing together. with increased levels of ill health now associated with obesity and inequality, will we see an increase in CVD, not to mention emotional ill health.
Born before the birth of the NHS, now watching its demise, I cannot help but compare the good and the bad, an age thing. People need to take responsibility for themselves, yes, but some have a raw deal. Great reading Dr Kendrick.

I’ve been following your blog for some time, Dr Kendrick, and honestly I’m amazed they haven’t tried to silence you yet, as is usually the case for people who drop truthbombs.

Angelica, Omeprazole is a nasty drug in the long term. I was on it for 6 years and it caused horrendous health problems. It all started when I was having random digestive trouble like episodes of vomiting because (and this is still the case) sometimes food won’t “go down” and stays in my stomach for hours. I don’t have indigestion or heartburn. GP sent me for an endoscopy. Grade C oesophagitis diagnosed and was told to take Omeprazole “for the rest of your life probably”. 40mg for 8 weeks going down to 20mg a day.

I was in a rather stressful job at the time and somewhere around this diagnosis I noticed other alarming symptoms. Firstly my feet began swelling until it was at the stage I couldn’t wear shoes any longer. The first GP I saw about this said “That’s a rather nasty food intolerance you’ve developed there” and I spent a whole year eliminating food groups without discovering what was causing the (by now) multiple symptoms.

My skin was almost permanently itchy and breaking out in hives. The swelling in my feet was at the extent I could only wear flip-flops. My hands began to swell too. Joint pain set in and it got to the point where I could barely walk or drag myself out of bed. I gave up work, saw multiple GPs and (long story short) was diagnosed with rheumatoid arthritis eventually.

So I was put on methotrexate, got splints for my seized-up hands, occupational therapy, steroid injections, etc. Methotrexate is an incredibly dangerous drug and made me horribly ill so the Omeprazole was increased. Steroids actually helped for a month or so, but nothing was working long term.

After about 5 years of being very unwell indeed I saw a different rheumatologist and was put on Sulfasalazine alongside the Methotrexate and discovered on Drugs.com that there isn’t a happy interaction between these drugs. I printed it out. Thank god I did because the website since reviewed the interaction and downgraded it. At this point I even thought “Are they trying to kill me?” I was more ill than ever, barely able to walk, having blood tests every month (which showed high inflammation, I believe, and anaemia but not much else), my hair was falling out.

And one day I just gave up on it all. I said to myself “These drugs are going to kill me. Let’s go back to the beginning and see if this is a food intolerance of some sort.” I wrote to my rheumatology nurse saying I was discharging myself from their care (the nurses were excellent by the way and absolutely faultless), sent them a print-out of the drug interactions and stopped taking everything that was prescribed. I took a cheap anti-allergy pill every day instead.

Within 7 days all my symptoms disappeared. Two years on and I’m still symptom-free.

Here’s the crazy thing. The only problem that remained was the original digestive trouble, so I was sent for another endoscopy this year and diagnosed with Grade D oesophagitis. It has got worse! And of course I was prescribed Omeprazole again. Within 2 days all the horrendous symptoms came back – huge swelling of feet and hands, hives and itching, joint pain, etc.

And that was the final lightbulb moment. You cannot imagine my relief. I experimented, came off it for a week, restarted it, symptoms returned. It had been a reaction to the Omeprazole all along. Phoned the GP who prescribed it. She said “Unusual, but it could be” and prescribed Lansoprazole instead. Wouldn’t you know it, this is also causing swelling, joint pain, etc although not to the same extent.

So now I’m unsure how to progress: the oesophagitis is very bad (numerous times food gets stuck and swallowing is painful if not impossible) and really must be treated. But I’m obviously intolerant of this group of drugs and I don’t think it’s even working. As you can imagine I’m rather wary of seeing any more doctors and have no idea where to go from here.

Sorry to hear of your circumstances Donna, but thanks for posting. I suspect I am well known for not knowing what I am talking about, so first don’t believe anything I say, at least without checking first. I think there are some starting points which I see as useful for many people, one is https://youtu.be/IwHQTwdPToc. John Bergman is hated by medical practicioners, and described as a quack, so he’s got street cred. 😸 Another person to look up is Barbara O’Neill who has many youtube videos. If you are in the UK someone who is also at the top of the list is Affifa Hamilton, and she has a website to visit. Those might be helpful.

Wow that’s amazing, DonnaBlack! Thanks for sharing! I also have issues with things getting stuck in my esophagus but I’ve always managed to get it cleared up. I have two suggestions for you, first is plain old baking soda, in small doses, not to cause a big reaction but a smaller one. I take about a quarter teaspoon at a time, which produces one tiny burp. I’ve done it about once an hour from 7pm (after dinner) to 10pm, before bed.

At times I’ve had my bed propped up at the head because it was so bad I felt like I couldn’t breathe when I lay down. I now put one pillow under my ribs (I sleep on my side) and two under my head for a much milder incline. Unfortunately that triggers my back sometimes, but I couldn’t deal with the incline.

Some years ago I was reading about the keto diet and realized that there seemed to be a connection between proton pump = stomach acid and proton pump = secondary energy production in mitochondria. At that point I also stopped omeprazole and had a revival of energy which smoothed out later. Honestly I don’t understand it, it’s too technical for me, but every time I tried to look up proton pump and what it does, I’d end up with an article about ATP or some sort of ATPase.

I don’t have the kind of severe reaction you had, but I do get very tired if I take any ppi for more than a few days. Those things are very bad news, I think. I only use them now if the baking soda trick didn’t work and then I limit it to two or three days.

Oh yeah, I also found that a TENS unit directed at my vagal nerve (in the neck) helped my stomach empty. But it must’ve been mild because after using it for a while, the sluggish-stomach stopped happening much. Now I would have to eat much too much food, to trigger the sluggish stomach effect. I think that’s an official medical practice for stomach emptying, but I’m not sure about every country’s local practices. It was categorized as a “biofeedback” technique in the US.

DonnaBlack, I would try, if I was you, a simple Low Carb Diet. I suffered with GERD for years and was prescribed Omeprazole long term, which didn’t really eliminate the problem. My symptoms were not nearly so severe as yours, in fact in comparison I was quite well, but I started to do The Atkins Diet, the old fashioned way, purely to lose weight. By the old fashioned way, I mean no shakes, bars and ready meals, just eat real food and very few carbohydrates.

Within days, long before I had any significant weight loss, my GERD had spontaneously resolved, my soaring high blood pressure was gradually reducing, my joint pains resolved, it was like a miracle! The only thing that went ‘wrong’ according to mainstream medical opinion, was that my Cholesterol (already pretty high) shot up. But thankfully, I discovered Dr Kendrick and basically ignored that!

So now I am medication free (apart from blood thinners as I had a severe DVT a few years later) but in every other respect I am fit, well and happy and 25kg lighter. I will be a ‘low carber’ for life!

So try eggs for breakfast, any old meat, fish and salad for lunch, with a good salad dressing or home made mayo, and any old meat fish and above ground vegetables for dinner, you can have creamy sauces (lemon juice, lemon zest and double cream added to pan juices of fish or chicken makes a luscious sauce). Avoid seed oils (so called vegetable oils, highly processed and inflammatory) and use butter, lard and olive oil for cooking / dressings.

Similar stories are all over the ‘low carb forums’. The modern highly processed diet is the cause of so many problems, I am sure.

I took omeprazole to counter the acid production caused by NSAIDS (a long story that began with a statin prescription), and when I finally got off everything, I was shocked to discover that I had heartburn. It would seem that the body becomes somewhat used to omeprazole and then overshoots the other way a bit when it is removed. I didn’t want to become addicted to anything else, so I used Gaviscon (which works mechanically to contain the stomach contents) and the problem subsided after about 2 weeks.

I was on this for years after graduating from Gaviscon. Originally I was hopeful that a low carb diet would help, but no luck – UNTIL I gave up wheat. Who knew? Well lots of people actually. I’d suggest wheat elimination first – after all contrary to what dieticians will tell you you won’t die without it – and if that fails try an old-fashioned H2 blocker, other factors may also be involved. Less profitable than PPIs but often with fewer side effects.

I gave up wheat too. After years of recurrent, severe heartburn I was able to pinpoint wheat as the culprit. It’s basically black and white — if I eat wheat I get heartburn, if I don’t eat wheat I don’t get heartburn.

N=thousands. I actually eliminated it when I found the only thing that spiked my blood glucose worse than wheat was wheat mixed with other carbs. The lack of GERD and also lack of farting was an added bonus.

For years I used to buy an oral steroid (indomthacin) over the counter for my ankylosing spondylitis. Then one day the pharmacist refused to supply me any more without a prescription. I was angry because I couldn’t afford a visit to the doctor for a script. So I took a tip from Goran Sjoberg and used turmeric instead, which seems to work almost as well.

Reading this article, it seems the pharmacist did me a big favour. He always warned me against stomach problems, which I never got, but never mentioned that steroids were a factor in CVD. Maybe he helped me dodge a big plaque-shaped bullet. *touches wood*

Thank you Dr. K for another great post! I remember pathology lectures in medical school about atherogenesis and subsequent remodeling. I also, remember being shushed by a drug rep for asking, “why would I take a statin drug that stops a normal process (cholesterol metabolism) that my liver is happy to do?” I can say that after residency I have not prescribed that class of drugs. Looking forward to your post on what we can do proactively to perhaps keep CVD at bay.

Excellent summary. I like the inflammation hypothesis as a CVD cause since this might be easier to fix. There are many factors involved leading up to inflammation.
Postprandial inflammation deserves a closer examination that is why I started a food intake diary listing foods consumed and time of day. Also take BP readings 2 times in a.m. and p.m..
Found that eating once or twice per day makes for a shorter list. If there is postprandial inflammation then eating less often allows more time for repair.

Ummmmmm..They do Kathy..A brand new Boeing 737 fell out of the sky and crashed just after take off near Jakarta, with no survivors a few weeks ago .. Turns out that the on board computer caused the crash and fought the pilots attempts to prevent the crash…170 people all dead… due to a high tech computer stuff up…

Bill in Oz: I was thinking about this, too (great comment, though!). Apparently stall-avoidance systems have been used on commercial aircraft for decades, and are not difficult to override. The 737 Max has a new version, and it seems Boeing failed to fully notify pilots of its operation. The cause of the crash will never be known for certain, but it may have been a combination of system failure and pilot error, or perhaps this particular plane’s system malfunctioned. My brother and I once flew seated in the same row with a 747 pilot. He told us that in the U.S., pilots are trained on a wide variety of aircraft, but among Asian airlines, it is more common to train them only on the model they will be flying. Better for contingencies, a wider variety of experience.

I recall that two Russian aircraft models similar to each other had (I think) brake pedals that operated in opposite directions. This was the cause of several crashes because the pilots reactions were incorrect for the situation. So sometimes good sometimes bad to be on different types, though in general I agree that experience on more types would allow better decision making.

Gary, I’ve often wondered if these new computer managed aircraft have a”Turn the bloody thing off ” button..On this model of the 737, apparently not.

By the way, enjoying exploring the real reasons behind climate warming and debunking the CO2 alarmists here in Oz..
‘Skepticism’ seems to be a necessary character trait..And DR K runs an excellent training is the development of skepticism !

Bill in Oz: Yes, I find it fascinating to learn climate science. The alarmist position is clearly a political one, not a scientific one. And the policy response by governments to the minor to non-existant warming caused by burning fossil fuels is causing great harm. The French are thoroughly pissed off.

Gary Ogden – the anti-alarmist position (“there’s nothing to worry about, everything’s fine”) is political. The filthy fuel industries have their PR departments at work all over the various media, and their money in the pockets of politicians in our government. I sincerely doubt that Trump’s denial of climate change has anything to do with science.

Mark Sanders: Correct. Most politicians, like most of the general public, misunderstand science. Earth’s climate is so complex that it is nearly impossible to see it whole, and data is sparse prior to the satellite era, except for proxies, such as ice and sediment cores, tree rings, etc. What is fairly certain is that nearly everything we’ve heard or read in the media about this issue is wrong. What I suggest to anyone interested in understanding climate science is to read it, immerse yourself in it. Politics and bias afflict nearly every institution, but there are still many honorable people doing real science.

Nice summary of the writings. Running in my mind is I wish more health care providers would consider this theory over the cholesterol theory and prescribing statins with the side effects they have. It could help people avoid unnecessary suffering I suspect.

My mom takes a statin. That came about after a check up with a doctor of course. Mom thinks very highly of doctors and the health care system. Doctors walk on water with her, which in all fairness seems to be how most feel in the US. The statin prescription came about a year ago I believe. Today, of late, mom has developed a great deal of trouble with her muscles and walking. I of course don’t know if the two are connected, taking a statin and her muscle pain. Possibly the statin is the cause. I suspect there is a chance and it should be investigated.

For the brief time I took a statin it caused me muscle and joint pain. I stopped soon after. I never had much faith in the cholesterol theory. A friend that took a statin, and a big believer in doctors, experienced similar. He took the statin muscle pain as long as he could till it became to much and then he stopped. Was a bit odd to me as later he was regretting that he went against his doctor’s wishes and stopped the statin.

Moms doctor is saying the walking pain problem is arthritis and that she will need a hip replacement surgery.

So far mom appears to be fighting this, looking at ideas to help her hip pain. I suggested avoiding medications and supplements she takes for a few days to see if they are the cause. The suggestion didn’t seem to go far. While sad, as a spectator of all this will be interesting to see how this plays out.

That was my thought also, standard diagnosis about the hip replacement.

Mom is now taking lots of NSiADS. The anti inflammatories are helping and has her walking again, as of the other day. Now of course I’m concerned about the anti-inflammatories causing her a heart attack.

If you believe that obesity/diabetes is connected to CVD and want to reverse this downhill race to the ultimate end, overwhelming clinical practice (and science) with LCHF is today all behind you but to the continuous dismay of Big Pharma/Agro.

I’m curious why you aren’t talking about the chronic scurvy connection as Linus Pauling put forth?
It appears to me that the chronic scurvy idea fits perfectly with the Thrombogenic theory that you favor. The fact that Pauling therapy as a treatment has a long history of extraordinary success adds credibility to his theory.

Daniel Cobb, (whose book I linked to above) says “In my clinic, we have a saying – that heart disease is easier to treat than low-back pain. Treating chronic scurvy nutritionally, because it directly addresses the cause, almost always works.”

I have discussed the Rath/Pauling hypothesis many times. I like it. If you note that vitamin C gets mention on my list of things that cause CVD. I have no problem with a low vitamin C as a cause of CVD. However, it is only A cause, not THE cause. If I have attempted to make one thing clear it is that the search for THE cause of CVD has led us to the position that we are now in. Namely, a confused mess.

I am so impressed about Pauling Therapy because it has such a high success rate, even with so many causes as you describe. I think it may be worth it for you to look at the book I linked to above to see the specific products and dosages used, which could be helpful for your next blog post about treatment.

Also, since clots form when the endothelium is stripped away and the blood comes in contact with Tissue Factor, what stops clots forming spontaneously in the absence of endothelial damage when the blood from the vasa vasorum comes in contact with the same TF? Or is TF only released as a result of endothelial damage?

The very first researchers saw cholesterol crystals in plaques. The assumption became that these crystals must have come from ‘cholesterol’ in the blood. LDL carries a high percentage of cholesterol. The next step was easy. The cholesterol crystals in plaque must have come from LDL. Wrong.

Also, remember that Lp(a) is attracted to areas of arterial damage. Lp(a) and LDL are identical apart from one protein attached to the side apolipoprotein (a). How do you tell the difference between LDL and Lp(a) when you find them in the artery wall? You must look for apolipoprotein (a). If you do, you find it is there. If you don’t, you think you are looking at LDL. When you are not.

Malcolm
I still don’t get it about Lp(a). If you have a high reading presume that means you need some repairs and the Lp(a) is doing it which is surely good and part of the natural process. I would rather be perfect, but my second choice is to have the natural product doing what it is meant for.
Where does this reasoning go wrongchris.harvey@?

Asthma can raise blood pressure, which would seem logical enough since the heart must work harder to get air through narrowed airways, something like that. Taking asthma medicine isn’t going to help blood pressure either since Salmeterol in Seretide is a beta stimulant which means it has the opposite effect to a beta blocker. I tend to get asthma when the weather is cold and damp. My blood pressure readings, taken by me on an Omron monitor, are high. Should I be worried about this when I know the reason? I really don’t want to ask my doctor who will just suggest more medicine and I will end up like the old woman who swallowed a fly.

“In humans and animals lacking functional LDL receptor (LDLR), LDL from plasma still readily traverses the endothelium…ALK1 mediates uptake of LDL into endothelial cells via an unusual endocytic pathway that diverts the ligand from lysosomal degradation and promotes LDL transcytosis. The endothelium-specific genetic ablation of Alk1 in Ldlr-KO animals leads to less LDL uptake into the aortic endothelium, showing its physiological role in endothelial lipoprotein metabolism…”

I’m chasing the references in the paper a bit, and there are some experiments with cholesterol-fed mice and rabbits (yeah, I know) showing plaque regression after LDL-reduction.

I doubt the finding of ALK1 really contradicts Dr. K’s statement “…that LDL cannot get into any cell, let alone an endothelial cell, unless that cell wants it to…”. But, it appears there’s an alternative to the LDL receptor, and the paper is a window into the mainstream view and why that view might persist.

So why does the LDL level go up to enormously high levels in homozygous FH? If, that is, cells do not actually need an LDL receptor for LDL to gain entry. As to how anyone knows that LDL traverses the endothelium in humans. That is not the sort of experiment that you can do in humans. At least not living humans. Also, I know that LDL cannot traverse endothelial cells in the brain, because the brain requires glial cells to synthesize cholesterol – as it cannot get any from the bloodstream. – because it cannot get past the BBB. This research reminds me of the planet Vulcan.

LA Bob: The answer might be in capillaries. Apparently cells need to be within 4 cell distance from a capillary. LDL must be able to exit capillaries and move across several cell layers. Maybe tight junctions are not as tight in capillaries as they are in larger blood vessels.

Gary Ogden: reference on how LDL particles can end up on the other side of endothelial cells. This confirms the possibility that precursors of fatty streaks can form in any tissue. Pimples and boils come to mind. Arteries with vasa vasorum would not be exempt.

Andy S: This is talking about the lymphatic system. Confusing, because they use the term lymphatic vasculature, and refer to its endothelium. Surely the lymphatic system is different from the blood circulatory system, or do I need to go back to kindergarten?

Gary Ogden: this article was referenced. The point is that LDL can end up on the other side of endothelial cells. Lymphatic system function is to return the extracellular stuff back into circulation. Capillary bed could be likely place that clogs up and junk accumulates. Possibly inflammation can start in different tissues at these clogged sites. Blood composition appears to be a driving force in disease.

https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4274060/
LDL and HDL transfer rates across peripheral microvascular endothelium agree with those predicted for passive ultrafiltration in humans
“We conclude that the transport of HDL and LDL from plasma into interstitial fluid across the peripheral vascular endothelium in healthy humans can be explained by ultrafiltration without invoking an additional active process such as transcytosis.”

I seem to only get a reply button once so can’t reply above. The responses re autoimmune were interesting and likely all play a part. The absence of microbes is a problem too. Vaccines with their many components and adjuvants may provoke immune system confusion. But it may also be an unknown microbe, such as I suspect in multiple sclerosis.

AnnaM: I believe one of the key issues driving autoimmunity and other conditions lies in the gut microbiome. Fascinating field. I’ve read enough about the microbial world that I would be skeptical to assign pathogenicity to a single species. I think Bechamp was correct, and much work is being done to validate his supposition that it is the host/microbe interaction which can trigger pathogenicity. Otherwise everyone would be sick all the time because we live in a sea of microbes all the time, gazillions of them.

Autoimmune diseases often seem to occur after an infection, like flu or measles. There’s a genetic factor involved in the “strength” of the immune system which would probably have been an advantage in areas with high levels of microbes (HLA antigens).

I’ve read two competing theories – either the lack of such infectious agents in the modern world causes the immune system to “go off on one” and attack the body’s own components when it has nothing else to fight. Alternatively there may be an “opportunistic infection” which only invades people who are already ill from something else, which may trigger an autoimmune attack. So may things like gluten if they get through the tight junctions in the gut and end up in the bloodstream. People with coeliac are more prone to Type 1 diabetes.

Add a lot of modern chemicals which we never evolved to process. And possibly a lack of vitamin D – some autoimmune diseases are commoner nearer to the poles than the equator. Like CVD it’s complicated . . .

Thank you Dr Kendrick for all your explanations. However, I wonder how many health professionals will move on from the scenarios they learned as students? To digest this info, then change the hard wiring of the status quo, is likely to take a generation. This week I was told emphatically that high LDL is the bogey man, and the way to avoid it is to minimise all dairy products and saturated fats, with no blame whatsoever being attached to refined carbohydrates. Oh, and there is now a great, new, injectable medication to solve the awful cholesterol problem(!).
Please keep plodding on….we all appreciate your commitment. I couldn’t begin to explain your work, but it clarifies in my mind why we must question out-moded regimes. I feel the public are being fobbed off with blasé retorts such as those I have mentioned above.

Jennifer, I wonder if it is worthwhile setting up a global list of ‘dopey bastards’ in the medical profession so that all of us across the English speaking part of the planet can avoid ever consulting them for their wisdom…

Now Bill, that sounds like an excellent scheme!
I find the staff nice, and they mean well, but many are convinced that the garbage they continue to spout out is up to date and correct. I suspect that if they were to read, then implement, the stuff we access on this wonderful blog, they would soon be unable to practice in the NHS.
I have now learned to follow what my Mother taught me as a child……just nod, say aye, yes and no…..then do as you think fit! Saves all the conflict, and keeps my blood pressure at bay.

Dr Kendrick asks why atherosclerotic plaques never form within the chambers of the heart?
My guess is it’s something to do with fluid dynamics. The weak points in a healthy heart are the valves, but no sooner than they come under increased pressure they open relieving this and preserving the chamber walls at their expense. Blood clots do not get a chance to form on the valves because they would be knocked off immediately. Calcification can occur, I believe, but I’m not sure what precisely calcifies.

Posting problems! It is well established, not least through archeology, that hunter gatherers were fare more healthy than those subsisting on grain diets where records tell about atherosclerotic plaques, e.g. found in mummies.

I am, as a “lover of serious books”, now deep down in a new released exceptional book touching on this subject: “Against the Grain, A Deep History of the Earliest States” by Professor James C. Scott involved as a codirector of the Agrarian Studies Program at Yale University.

This book is very much about the health deterioration, not least through epidemics partly due to compromised immune resistance, that occurred in the transition from hunting and gathering to sedentary mono-crop agriculture state level scale, first in Mesopotamia about five thousand years ago.

This book is to me making things very understandable in the same way as Malcolm’s present post on CVD. In essence it is a great summary of what I have come across during twenty years of scrutinizing the CVD-health/food issue.

I think there are too many confounders in transition from hunter gatherers to agriculture to suggest that health deterioration is due to one factor (grains). And since it was members of upper classes who were usually mummified, they had vastly different lifestyles from that of hunter gatherers. IMO, you’re comparing apples to oranges…

Also, grain consumption existed in hunter gatherers and probably intensified long before Mesopotamia 5 thousands years ago as wheat was domesticated around 9,000 BCE and millet around 6,000 BCE to use just two examples.

Pre-neolithic hunter-gatherers, in some cases, ate some grains. But no where near at the level of the neolithic agriculturalists. Also, during this time, grains were radically changing through cultivation. As for the Egyptian elite, they were eating more grains than anyone, as farmers were still forced to partly subsist from hunting, fishing, and gathering.

I think Egyptian elite ate more of everything than anyone, not just grains. Also, their lifestyle was radically different from that of commoners or hunter gatherers. So, my point was that when we compare rates of atherosclerosis in Egyptian mummies to those of hunter gatherers and link them to grains alone, we probably ignore a number of other factors that may have contributed.

Sasha, you are quite right that cereals were domesticated early but it is a fact that it took the states to be solely based on grain (this is one of the main points in Scotts intriguing book) several thousands of years, maybe as many as 7 000, to be established as proper states, e.g. Uruk or Ur.

So grains during this extended period of time was basically an addition to a varied diet if I shall believe Professor Scott and he seems to know what he is talking about. Agriculture based on grain was a means by which the elites took control over people and food – taxation, grain, was central for their staying in power. Interesting enough this control over agriculture and people is even a more obvious fact today.

Interesting reading indeed and with your pronounced interest in this subject I suggest that you get a copy of the book and I am sure you will not get disappointed.

Goran, thank you. I actually have the book and read about 20 percent of it (I have an unfortunate tendency to jump from book to book without finishing). I plan to return to it in the future.
I find the idea that agriculture, and grain cultivation in particular, led to the development of states and class societies to be very interesting and it’s repeated by a number of scientists. Maybe that’s why Jared Diamond called agriculture “possibly the worst mistake of humankind”.

However, I think that most people’s interest in grains relates to health and lifespan. I have been looking into the arguments for and against carbs and grains since coming across LCHF hypothesis that carbs and grains are detrimental to health. In my opinion, there’s enough epidemiological data to question at least some of that hypothesis: Kitavans and high carb consumption, Okinawans and sweet potatoes, southern Italians and pasta, to use just a few examples.

There are also some researchers like Stephan Guyenet and Valter Longo who are worth looking into if one is interested in longevity and health spans. Dr. Guyenet, for example, has a very interesting book “The Hungry Brain” that looks into evolutionary drives for weight gain and metabolic illnesses. On a recent podcast with Chris Kresser Dr. Guyenet discusses Gary Taubes’ recent book “The Case Against Sugar”. While he’s careful to say that he’s not there to exonerate sugar, Dr Guyenet says that he read the book and is familiar with all evidence Taubes cites but he still doesn’t understand how Taubes comes up with some of his conclusions.

I think we all are susceptible to confirmation biases and linear thinking and it’s important to keep those in mind if we want to understand.

@Göran – I’d take the argument much further forward into history. We know from records that, through the 19th century, Americans were eating more meat than bread. Vegetable and fruit consumption was also relatively low and mostly seasonal. Part of that is because gardening was difficult with so many pests.

With so much natural areas around, hunting and gathering remained a large part of the American diet. Even in the cities, wild game was easily obtained at cheap prices. Even into the 20th century, hunting and gathering was still important and sustained many families through the Great Depression and the world wars when many foods were scarce.

It was different in Europe, though. Mass urbanization happened centuries before it happened in the United States. And not much wilderness was left standing in recent history. But with the fall of the Roman Empire and into feudalism, many Europeans returned to a fair amount of hunting and gathering, during which time general health improved in the population. Restrictive laws about land use eventually made that difficult and the land enclosure movement made it impossible for most Europeans.

Even so, all of that is fairly recent in the big scheme of things. It took many millennia of agriculture before it more fully replaced hunting, fishing, trapping, and gathering. In places like the United States, that change is well within living memory. When some of my ancestors immigrated here in the 1600s, Britain and Europe still maintained plenty of procuring of wild foods to support their populations. And once here, wild foods were even more plentiful and a lot less work than farming.

Many early American farmers didn’t grow food so much for their own diet as to be sold on the market, sometimes in the form of the popular grain-based alcohols. It was in making alcohol that rural farmers were able to get their product to the market without it spoiling. I’m just speculating, but alcohol might have been the most widespread agricultural food of that era because water was often unsafe to drink.

Beta blockers are used as part of a standard post ACS meds. Bisporolol very common. Nothing to do with cholesterol, but simply to reduce the workload of the heart. They are also used to treat anxiety and lower BP.

It may not be just a simple allergy (if such a thing can be simple) to gluten. There appears to be a sub-clinical condition where the agglutin has an association with leaky gut, and so unwanted components can pass into the blood. This seems to have increased coincident with the introduction of the modern, 56 chromasome, high yeilding wheat, (and possibly compounded by the use of glyphosate spray to dessicate it just before harvest). Stephanie Seneff is a useful source.

Andy, people are free to eat whatever they wish, of course. But I think that most researchers would tell you that you can’t claim causation based on what you wrote. I am fairly certain, that you can find vegan stories on the Internet that claim something similar to your experience.

Sasha: That was just an observation that got me thinking. I now believe that most diseases have inflammation as the initiating cause. Cells that experience dyshomeostasis produce cytokines (signal molecules) that alert the immune system to go into action. I also believe that there must be a homeostat system that governs the functions of the different systems to maintain homeostasis.

Andy, if all grains are inflammatory to everyone at all times, it would mean that grain-based societies are at evolutionary disadvantage (on the level of an individual) to those societies that consume no grains. Is there evidence for this?

And also, why would nature not make adjustments for this, the way it did with dairy?

Yes, already in the famous Gilgamesh epos (the first book proper) it is mentioned how “the wild man”, Enkidu, was civilized or rather captured through the “temptation” of a combination of “bread, alcohol and a prostitute” – I can agree on the first two parts.

I am sure you would also enjoy this new book – it is great reading in my eyes; actually one of the best I have read for long.

Grain these days is cheap thanks to Big Ag and mechanization. It wasn’t always so. If the fields had to be ploughed by draught animals, and the grain weeded, harvested, and threshed by hand, the final product was expensive. Grain became a store of value and a medium of exchange. Eating grains was literally like eating money, so presumably they kept consumption to a minimum.

I think it’s true of all food groups, not just grains. We often fail to realize how much our food environment changed in the last 100 years or so, at least in the developed world, and not just in quality but in quantity. I remember what it was like in the Soviet Union before the end of Cold War, about only 30 years ago. It is very different today in major Russian cities and it shows in peoples’ expanding waistlines. The other day I was buying food at a large market in Moscow, one of 5 or 6 of its kind, in addition to thousands of supermarkets, minimarkets, food stalls and eateries that are now at every corner here. I stood there looking at vast amounts of food, remembering my very different young years before the end of the Soviet Union and I was wondering: who eats all this stuff? According to business people, the sanctions are definitely having an effect on the Russian economy but one thing is virtually certain in my opinion: whatever happens next, Russians are not about to die from hunger…

I think that in the developed world we are all fighting an uphill battle in light of our evolutionary drives for sugar, fats, and protein. On this topic I would again refer to Dr Guyenet’s excellent book “The Hungry Brain”.

@Sasha – “I think Egyptian elite ate more of everything than anyone, not just grains.”

That is a reasonable speculation. But I’m not sure. The poor ate fairly well in many societies, specifically when they had access to wild sources of food. That would have been the determinant of health for the Egyptian poor. I would imagine, for example, that the average Egyptian had a diet rich in fish from the Nile river.

“Also, their lifestyle was radically different from that of commoners or hunter gatherers.”

That much is for certain.

“So, my point was that when we compare rates of atherosclerosis in Egyptian mummies to those of hunter gatherers and link them to grains alone, we probably ignore a number of other factors that may have contributed.”

Yeah, most things are more complex than they typically get portrayed. I don’t doubt that it would be true in this case as well.

The Egyptian ruling elite probably ate a fairly healthy diet or at least healthy according to the claims of official dietary recommendations. Besides lots of agricultural foods, I bet they were also getting plenty of nutrient-dense foods, even a fair amount that was hunted and gathered. The physical inactivity might have played the largest part.

But it’s possible the poor were eating more of at least certain wild foods and other nutrient-dense food that had gained a stigma of being poor people’s food. For example, not that long ago, lobster and liver were seen as signs of low class.

Benjamin, I agree with a lot of your points, except with your assertion that “the poor ate fairly well in many societies especially when they had access to wild sources of food”. I know how the poor ate in Russia in the beginning of the 20th century and how the poor eat now in the former Soviet republics and in India. Their diet is very poor even though they can have access to wild sources of food.

I don’t know what the situation was for the poor in ancient Egypt but I would be very surprised if it was better than in modern day India or former Soviet Union.

Another factor in Egyptian elite’s atherosclerosis could have been 24/7 availability of food.

The most obvious example are hunter-gatherers, poor by standards of modern industrialization while maintaining great health, as long as they their traditional way of life is able to be maintained. Many populations that are materially better of in terms of a capitalist society (access to comfortable housing, sanitation, healthcare, an abundance of food in grocery stores, etc) are not better off in terms of chronic diseases.

As the main example I already mentioned, poor Americans have often been a quite healthy lot, as compared to other populations around the world. It is true that poor Americans weren’t particularly healthy in the early colonial period, specifically in Virginia because of indentured servitude. And it’s true that poor Americans today are fairly bad off. Yet for the couple of centuries or so in between, they were doing quite well in terms of health, with lots of access to nutrient-dense wild foods. That point is emphasized by looking at other comparable populations at the time, such as back in Europe.

Let’s do some other comparisons. The poor in the Roman Empire did not do well, even when they weren’t enslaved. That was for many reasons, such as growing urbanization. So, when the Roman Empire fell, many of the urban centers collapsed. The poor returned to a more rural lifestyle that depended on more wild foods. Studies done on their remains show their health improved during that time. Then at the end of feudalism, with the enclosure movement and the return of mass urbanization, health went back on a decline.

Now I’ll consider the early Egyptians. I’m not sure if there is any info about the diet and health of poor Egyptians. But clearly the ruling class had bad health. It’s hard to make comparisons between then and now, though, because it was an entire different kind of society. The early Bronze Age civilizations were mostly small city-states that lacked much hierarchy. Early Egypt didn’t even have the most basic infrastructure such as maintained roads and bridges. And the most recent evidence indicates that the pyramid workers weren’t slaves but instead worked freely and seem to have fed fairly well. The fact that the poor weren’t mummified leaves us with scant evidence that would more directly inform us.

On the other hand, no one can doubt that there have been plenty of poor populations who had truly horrific living standards with much sickness, suffering, and short lifespans. That is particularly true over the millennia as agriculture became ever more central, since that meant periods of abundance alternating with periods of deficiency and sometimes starvation. That was less the case for the earlier small city-states surrounded by the near constant abundance of wilderness areas.

As always, it depends on what are the specifics we are talking about. Also, it is relative.

My mother grew up in a family that hunted and at the time there was a certain amount of access to natural areas for many Americans, something that helped many Americans get through the Great Depression and world war era. Nonetheless, by the time of my mother’s childhood, overhunting had depleted most of the wild game (bison, bear, deer, etc were no longer around) and so her family relied on less optimal foods such as squirrel, raccoon, opossum, and fish (the latter probably coming from highly polluted waters because of the very factories and railroad her family worked in). So, the hunting wasn’t nearly as good as it had been a half century earlier.

Being poor today means a lot of things that it didn’t mean a century ago or a millennia ago. The high rates of heavy metal toxicity today has rarely been seen among previous poor populations. Today 40% of the global deaths are caused by air pollution, primarily effecting the poor, also extremely different from the past. Beyond that, inequality has grown larger than ever before and that has been strongly correlated to high rates of stress, disease, homicides, and suicides. Such inequality is also seen in terms of climate change, droughts, refugee crises, and war/occupation.

I’d imagine Russia has far high inequality similar to the US. About India, that is one of the most impoverished, densely populated, and malnourished societies around. And modern industrialization did major harm to Hindu Indians because studies show that traditional vegetarians got a fair amount of nutrients from the insects that were mixed in with pre-modern agricultural goods. Both Russia and India have other problems related to neoliberalism that wasn’t a factor in the past. It’s an entirely different kind of poverty these days. Even if some Russians have some access to wild foods, I’m willing to bet they have no where near the access that was available in previous generations, centuries, and millennia.

Compare modern poverty to that of feudalism. At least in England, feudal peasants were guaranteed to be taken care of in hard times. The Church, a large part of local governance at the time, was tasked with feeding and taking care of the poor and needy, from orphans to widows. They were tight communities that took care of their own, something that no longer exists in most of the world where the individual is left to suffer and struggle. Present Social Darwinian conditions are not the norm for human societies across history. The present breakdown of families and communities is historically unprecedented.

There are lots of ways to get proper nutrients in any society: hunter gatherer, pastoral, or agricultural. The reasons poor often fail to get proper nutrition are as varied as the reasons they became poor or have stayed poor for generations.

In my opinion, all three macronutrients have a role to play in proper nutrition and I disagree with idealogically driven debates around it: LCHF vs LFHC, vegan vs carnivorous diet, no-grains vs mostly grains, and every other shade in between. I think I understand why people get attached to a particular diet but that doesn’t make their arguments evidence based, as far as I can tell. It has become almost like a religious or political debate, except that many religious people have been at it long enough to know better; something that can’t be said about various warring diet factions…

I don’t understand the relationship of your comment to my comment. I never claimed to advocate for some particular diet as a dogmatic ideology. I’ve tried many diets over the years. I’m familiar with the arguments and evidence from many perspectives. I am on a paleo diet at the moment, but I’ve been on a vegetarian diet in the past and the larger framework of my thinking is traditional foods.

I’m informed by the work of Weston A. Price which gave examples of health populations living in different places with different diets and lifestyles, even as they had certain things in common such as nutrient density. I’m willing to bet, though, that most of them had access to natural areas for hunting and gathering. For example, Price spent time with some isolated rural Europeans who were agriculturalists, but in being rural they probably ate some wild foods as well and their cows grazed on wild pasture lands.

Anyway, my opinion about diet is largely irrelevant in terms of my previous comments. I was focusing on the historical record, at least as I know it. I’ve been studying history, anthropology, etc for far longer and in greater depth than I’ve directly studied diet and nutrition. I don’t particularly care one way or another about dietary wars, per se.

My comment about diet wars wasn’t directed at you. I apologize if it created that impression.
On this blog we often have diet arguments because people are looking for ways to improve their health. My comment was in relation to that.

I don’t remember how we got to discussing the diet of ancient Egyptians but it could have been as a result of one of those diet arguments…

There are lots of ways of getting nutrients. But not all ways are equal. That is why discussing the scientific evidence is so important.

Someone can argue a particular food has high levels of a nutrient. But what matters is the bioavailability of that nutrient, which involves complex other factors. Our total health, diet, and lifestyle also determine how well we absorb, process, and make use of nutrients. That is the importance of understanding a historical and evolutionary perspective.

Taking industrialized foods that are denatured and then adding back in a few vitamins won’t be comparable to the original state of the food. For example, homogenized, pasteurized low-fat milk with added vitamin D that is common today vs the raw dairy foods from pastured cows that was eaten by some of the populations Price studied.

No matter what diet any of us is on and no matter what any of us believes, the science is simply what it is and the historical record is what it is. It is useful information for us to learn from.

Everything about present populations is extremely abnormal. In World War II, the US government had to reject 40% of recruits because of manourishment. So, what had happened to the health of the population?

Well, there were many changes. Overhunting made many wild game species extinct or eliminated them from local areas. Also, a new form of enclosure movement happened as laws were passed to prevent people from hunting and foraging wherever they wanted (early American laws often protected the rights of anyone to hunt, forage plants, collect timber, etc from any land that was left open, whether or not it was owned by someone).

That was combined with mass urbanization and industrialization with all of its new forms of pollution, stress, and inequality. Processed foods were becoming more widespread at the time. Around the turn of the century unhealthy and industrialized vegetable oils became heavily marketed and hence popular, which replaced butter and lard. Also, muckraking about the meat industry scared Americans off from meat and consumption precipitiously dropped.

So, in the decades prior to World War II, the American diet had already shifted toward what we now know. A new young generation had grown up on that diet and those young people were the ones showing up as recruits for the military. This new diet in such a short period had caused mass malnourishment.

Government officials and health authorities blamed it on bread production. Refined flour had become widely available because of industrialization. This removed all the nutrients that gave any health value to bread. So, there was a movement to fortify bread, initially enforced by federal law and later by state laws.

That helped some, but obviously the malnourishment was caused by many other factors that weren’t appreciated by most at the time, even though this was the same period when Weston A. Price’s work was published. Nutritional science was young at the time.

@Dr. Malcolm Kendrick – You write that, “Other mummies around the world, including hunter gatherers, also show calcified atherosclerotic plaques.” About that research, here is the relevant part from a lengthy analysis I wrote:

Now let me discuss the one group, the Unangan, that at first glance stands out from the rest. The authors say that the, “five Unangan people living in the Aleutian Islands of modern day Alaska (ca 1756–1930 CE, one excavation site).” Those mummies are far different than those from the other populations that came much earlier in history. Four of the Unangan died around 1900 and one around 1850. Why does that matter? Well, for the reason that their entire world was being turned on its head at that time. The authors claim that, “The Unangan’s diet was predominately marine, including seals, sea lions, sea otters, whale, fish, sea urchins, and other shellfish and birds and their eggs. They were hunter-gatherers living in barabaras, subterranean houses to protect against the cold and fierce winds.” They base this claim on the assumption that these particular mummified Unangan had been eating the same diet as their ancestors for thousands of years, but the evidence points in the opposite direction.

Questioning this assumption, Jeffery Gerber explains that, “During life (before 1756–1930 CE) not more than a few short hundred years ago, the 5 Unangan/Aleut mummies were hardly part of an isolated group. The Fur Seal industry exploded in the 18th century bringing outside influence, often violent, from countries including Russia and Europe. These mummies during life, were probably exposed to foods (including sugar) different from their traditional diet and thus might not be representative of their hunter-gatherer origins” (Mummies, Clogged Arteries and Ancient Junk Food). One might add that, whatever Western foods that may have been introduced, we do know of another factor — the Government of Nunavat official website states that, “European whalers regularly travelled to the Arctic in the late 17th and 18th century. When they visited, they introduced tobacco to Inuit.” Why is that significant? Tobacco is a known risk factor for atherosclerosis. Gideon Mailer and Nicola Hale, in their book Decolonizing the Diet, elaborate on the colonial history of the region (pp. 162-171):

“On the eve of Western contact, the indigenous population of present-day Alaska numbered around 80,000. They included the Alutiiq and Unangan communities, more commonly defined as Aleuts, Inupiat and Yupiit, Athabaskans, and the Tinglit and Haida groups. Most groups suffered a stark demographic decline from the mid-eighteenth century to the mid-nineteenth century, during the period of extended European — particularly Russian — contact. Oral traditions among indigenous groups in Alaska described whites as having taken hunting grounds from other related communities, warning of a similar fate to their own. The Unangan community, numbering more than 12,000 at contact, declined by around 80 percent by 1860. By as early as the 1820s, as Jacobs has described, “The rhythm of life had changed completely in the Unangan villages now based on the exigencies of the fur trade rather than the subsistence cycle, meaning that often villages were unable to produce enough food to keep them through the winter.” Here, as elsewhere, societal disruption was most profound in the nutritional sphere, helping account for the failure to recover population numbers following disease epidemics.

“In many parts of Alaska, Native American nutritional strategies and ecological niches were suddenly disrupted by the arrival of Spanish and Russian settlers. “Because,” as Saunt has pointed out “it was extraordinarily difficult to extract food from the challenging environment,” in Alaska and other Pacific coastal communities, “any disturbance was likely to place enormous stress on local residents.” One of indigenous Alaska’s most important ecological niches centered on salmon access points. They became steadily more important between the Paleo-Eskimo era around 4,200 years ago and the precontact period, but were increasingly threatened by Russian and American disruptions from the 1780s through the nineteenth century. Dependent on nutrients and omega fatty acids such as DHA from marine resources such as salmon, Aleut and Alutiiq communities also required other animal products, such as intestines, to prepare tools and waterproof clothing to take advantage of fishing seasons. Through the later part of the eighteenth century, however, Russian fur traders and settlers began to force them away from the coast with ruthless efficiency, even destroying their hunting tools and waterproof apparatus. The Russians were clear in their objectives here, with one of their men observing that the Native American fishing boats were “as indispensable as the plow and the horse for the farmer.”

“Here we are provided with another tragic case study, which allows us to consider the likely association between disrupted access to omega-e fatty acids such as DHA and compromised immunity. We have already noted the link between DHA, reduced inflammation and enhanced immunity in the millennia following the evolution of the small human gut and the comparatively larger human brain. Wild animals, but particularly wild fish, have been shown to contain far higher proportions of omega-3 fatty acids than the food sources that apparently became more abundant in Native American diets after European contact, including in Alaska. Fat-soluble vitamins and DHA are abundantly found in fish eggs and fish fats, which were prized by Native Americans in the Northwest and Great Lakes regions, in the marine life used by California communities, and perhaps more than anywhere else, in the salmon products consumed by indigenous Alaskan communities. […]

“In Alaska, where DHA and vitamin D-rich salmon consumption was central to precontact subsistence strategies, alongside the consumption of nutrient-dense animal products and the regulation of metabolic hormones through periods of fasting or even through the efficient use of fatty acids or ketones for energy, disruptions to those strategies compromised immunity among those who suffered greater incursions from Russian and other European settlers through the first half of the nineteenth century.

“A collapse in sustainable subsistence practices among the Aleuts of Alaska exacerbated population decline during the period of Russian contact. The Russian colonial regime from the 1740s to 1840s destroyed Aleut communities through open warfare and by attacking and curtailing their nutritional resources, such as sea otters, which Russians plundered to supply the Chinese market for animal skins. Aleuts were often forced into labor, and threatened by the regular occurrence of Aleut women being taken as hostages. Curtailed by armed force, Aleuts were often relocated to the Pribilof Islands or to California to collect seals and sea otters. The same process occurred as Aleuts were co-opted into Russian expansion through the Aleutian Islands, Kodiak Island and into the southern coast of Alaska. Suffering murder and other atrocities, Aleuts provided only one use to Russian settlers: their perceived expertise in hunting local marine animals. They were removed from their communities, disrupting demography further and preventing those who remained from accessing vital nutritional resources due to the discontinuation of hunting frameworks. Colonial disruption, warfare, captivity and disease were accompanied by the degradation of nutritional resources. Aleut population numbers declined from 18,000 to 2,000 during the period of Russian occupation in the first half of the nineteenth century. A lag between the first period of contact and the intensification of colonial disruption demonstrates the role of contingent interventions in framing the deleterious effects of epidemics, including the 1837-38 smallpox epidemic in the region. Compounding these problems, communities used to a relatively high-fat and low-fructose diet were introduced to alcohol by the Russians, to the immediate detriment of their health and well-being.”

The traditional hunter-gatherer diet, as Mailer and Hale describe it, was high in the nutrients that protect against inflammation. The loss of these nutrients and the simultaneous decimation to the population was a one-two punch. Without the nutrients, their immune systems were compromised. And with their immune systems compromised, they were prone to all kinds of health conditions, probably including heart disease which of course is related to inflammation. Weston A. Price, in Nutrition and Physical Degeneration, observed that morbidity and mortality of health conditions such as heart disease rise and fall with the seasons, following precisely the growth and dying away of vegetation throughout the year (which varies by region as do the morbidity and mortality rates; the regions of comparison were in the United States and Canada). He was able to track this down to the change of fat soluble vitamins, specifically vitamin D, in dairy. When fresh vegetation was available, cows ate it and so produced more of these nutrients and presumably more omega-3s at the same time.

Prior to colonization, the Unang would have had access to even higher levels of these protective nutrients year round. The most nutritious dairy taken from the springtime wouldn’t come close in comparison to the nutrient profile of wild game. I don’t know why anyone would be shocked that, like agricultural populations, hunter-gatherers also experience worsening health after loss of wild resources. Yet the authors of the mummy studies act like they made a radical discovery that throws to the wind every doubt anyone ever had about simplistic mainstream thought. It turns out, they seem to be declaring, that we are all victims of genetic determinism after all and so toss out your romantic fairy tales about healthy primitives from the ancient world. The problem is all the evidence that undermines their conclusion, including the evidence that they present in their own paper, that is when it is interpreted in full context.

As if responding to researchers, Mailer and Hale write (p. 186): “Conditions such as diabetes are thus often associated with heart disease and other syndromes, given their inflammatory component. They now make up a huge proportion of treatment and spending in health services on both sides of the Atlantic. Yet policy makers and researchers in those same health services often respond to these conditions reactively rather than proactively — as if they were solely genetically determined, rather than arising due to external nutritional factors. A similarly problematic pattern of analysis, as we have noted, has led scholars to ignore the central role of nutritional change in Native American population loss after European contact, focusing instead on purportedly immutable genetic differences.”

@Göran – I own a copy of Scott’s Against the Grain. But I’ve only skimmed some of it. I’m sure I’ll enjoy reading more of it.

Below is a passage that might interest you. It puts into context how extremely unusual has been the high-carb, low-fat diet these past few generations. This is partly what informed my previous comments.

We so quickly forget that the present dominance of a grain-based diet wasn’t always the case, likely not even in most agricultural societies until quite recently. In fact, the earlier American diet is still within living memory, although those left to remember it are quickly dying off.

The Big Fat Surprise
by Nina Teicholz
pp. 123-131

How Americans Used to Eat

Yet despite this shaky and often contradictory evidence, the idea that red meat is a principal dietary culprit has thoroughly pervaded our national conversation for decades. We have been led to believe that we’ve strayed from a more perfect, less meat-filled past. Most prominently, when Senator McGovern announced his Senate committee’s report, called Dietary Goals , at a press conference in 1977, he expressed a gloomy outlook about where the American diet was heading. “Our diets have changed radically within the past fifty years,” he explained, “with great and often harmful effects on our health.” Hegsted, standing at his side, criticized the current American diet as being excessively “rich in meat” and other sources of saturated fat and cholesterol, which were “linked to heart disease, certain forms of cancer, diabetes and obesity.” These were the “killer diseases,” said McGovern. The solution, he declared, was for Americans to return to the healthier, plant-based diet they once ate.

The New York Times health columnist Jane Brody perfectly encapsulated this idea when she wrote, “Within this century, the diet of the average American has undergone a radical shift away from plant-based foods such as grains, beans and peas, nuts, potatoes, and other vegetables and fruits and toward foods derived from animals—meat, fish, poultry, eggs and dairy products.” It is a view that has been echoed in literally hundreds of official reports.

The justification for this idea, that our ancestors lived mainly on fruits, vegetables, and grains, comes mainly from the USDA “food disappearance data.” The “disappearance” of food is an approximation of supply; most of it is probably being eaten, but much is wasted, too. Experts therefore acknowledge that the disappearance numbers are merely rough estimates of consumption. The data from the early 1900s, which is what Brody, McGovern, and others used, are known to be especially poor. Among other things, these data accounted only for the meat, dairy, and other fresh foods shipped across state lines in those early years, so anything produced and eaten locally, such as meat from a cow or eggs from chickens, would not have been included. And since farmers made up more than a quarter of all workers during these years, local foods must have amounted to quite a lot. Experts agree that this early availability data are not adequate for serious use, yet they cite the numbers anyway, because no other data are available. And for the years before 1900, there are no “scientific” data at all.

In the absence of scientific data, history can provide a picture of food consumption in the late eighteenth to nineteenth century in America. Although circumstantial, historical evidence can also be rigorous and, in this case, is certainly more far-reaching than the inchoate data from the USDA. Academic nutrition experts rarely consult historical texts, considering them to occupy a separate academic silo with little to offer the study of diet and health. Yet history can teach us a great deal about how humans used to eat in the thousands of years before heart disease, diabetes, and obesity became common. Of course we don’t remember now, but these diseases did not always rage as they do today. And looking at the food patterns of our relatively healthy early-American ancestors, it’s quite clear that they ate far more red meat and far fewer vegetables than we have commonly assumed.

Early-American settlers were “indifferent” farmers, according to many accounts. They were fairly lazy in their efforts at both animal husbandry and agriculture, with “the grain fields, the meadows, the forests, the cattle, etc, treated with equal carelessness,” as one eighteenth-century Swedish visitor described. And there was little point in farming since meat was so readily available.

The endless bounty of America in its early years is truly astonishing. Settlers recorded the extraordinary abundance of wild turkeys, ducks, grouse, pheasant, and more. Migrating flocks of birds would darken the skies for days . The tasty Eskimo curlew was apparently so fat that it would burst upon falling to the earth, covering the ground with a sort of fatty meat paste. (New Englanders called this now-extinct species the “doughbird.”)

In the woods, there were bears (prized for their fat), raccoons, bobolinks, opossums, hares, and virtual thickets of deer—so much that the colonists didn’t even bother hunting elk, moose, or bison, since hauling and conserving so much meat was considered too great an effort. IX

A European traveler describing his visit to a Southern plantation noted that the food included beef, veal, mutton, venison, turkeys, and geese, but he does not mention a single vegetable. Infants were fed beef even before their teeth had grown in. The English novelist Anthony Trollope reported, during a trip to the United States in 1861, that Americans ate twice as much beef as did Englishmen. Charles Dickens, when he visited, wrote that “no breakfast was breakfast” without a T-bone steak. Apparently, starting a day on puffed wheat and low-fat milk—our “Breakfast of Champions!”—would not have been considered adequate even for a servant.

Indeed, for the first 250 years of American history, even the poor in the United States could afford meat or fish for every meal. The fact that the workers had so much access to meat was precisely why observers regarded the diet of the New World to be superior to that of the Old. “I hold a family to be in a desperate way when the mother can see the bottom of the pork barrel,” says a frontier housewife in James Fenimore Cooper’s novel The Chainbearer.

Like the primitive tribes mentioned in Chapter 1, Americans also relished the viscera of the animal, according to the cookbooks of the time. They ate the heart, kidneys, tripe, calf sweetbreads (glands), pig’s liver, turtle lungs, the heads and feet of lamb and pigs, and lamb tongue. Beef tongue, too, was “highly esteemed.”

And not just meat but saturated fats of every kind were consumed in great quantities. Americans in the nineteenth century ate four to five times more butter than we do today, and at least six times more lard. X

In the book Putting Meat on the American Table , researcher Roger Horowitz scours the literature for data on how much meat Americans actually ate. A survey of eight thousand urban Americans in 1909 showed that the poorest among them ate 136 pounds a year, and the wealthiest more than 200 pounds. A food budget published in the New York Tribune in 1851 allots two pounds of meat per day for a family of five. Even slaves at the turn of the eighteenth century were allocated an average of 150 pounds of meat a year. As Horowitz concludes, “These sources do give us some confidence in suggesting an average annual consumption of 150–200 pounds of meat per person in the nineteenth century.”

About 175 pounds of meat per person per year! Compare that to the roughly 100 pounds of meat per year that an average adult American eats today. And of that 100 pounds of meat, more than half is poultry—chicken and turkey—whereas until the mid-twentieth century, chicken was considered a luxury meat, on the menu only for special occasions (chickens were valued mainly for their eggs). Subtracting out the poultry factor, we are left with the conclusion that per capita consumption of red meat today is about 40 to 70 pounds per person, according to different sources of government data—in any case far less than what it was a couple of centuries ago.

Yet this drop in red meat consumption is the exact opposite of the picture we get from public authorities. A recent USDA report says that our consumption of meat is at a “record high,” and this impression is repeated in the media. It implies that our health problems are associated with this rise in meat consumption, but these analyses are misleading because they lump together red meat and chicken into one category to show the growth of meat eating overall, when it’s just the chicken consumption that has gone up astronomically since the 1970s. The wider-lens picture is clearly that we eat far less red meat today than did our forefathers.

Meanwhile, also contrary to our common impression, early Americans appeared to eat few vegetables. Leafy greens had short growing seasons and were ultimately considered not worth the effort. They “appeared to yield so little nutriment in proportion to labor spent in cultivation,” wrote one eighteenth-century observer, that “farmers preferred more hearty foods.” Indeed, a pioneering 1888 report for the US government written by the country’s top nutrition professor at the time concluded that Americans living wisely and economically would be best to “avoid leafy vegetables,” because they provided so little nutritional content. In New England, few farmers even had many fruit trees, because preserving fruits required equal amounts of sugar to fruit, which was far too costly. Apples were an exception, and even these, stored in barrels, lasted several months at most.

It seems obvious, when one stops to think, that before large supermarket chains started importing kiwis from New Zealand and avocados from Israel, a regular supply of fruits and vegetables could hardly have been possible in America outside the growing season. In New England, that season runs from June through October or maybe, in a lucky year, November. Before refrigerated trucks and ships allowed the transport of fresh produce all over the world, most people could therefore eat fresh fruit and vegetables for less than half the year; farther north, winter lasted even longer. Even in the warmer months, fruit and salad were avoided, for fear of cholera. (Only with the Civil War did the canning industry flourish, and then only for a handful of vegetables, the most common of which were sweet corn, tomatoes, and peas.)

Thus it would be “incorrect to describe Americans as great eaters of either [fruits or vegetables],” wrote the historians Waverly Root and Richard de Rochemont. Although a vegetarian movement did establish itself in the United States by 1870, the general mistrust of these fresh foods, which spoiled so easily and could carry disease, did not dissipate until after World War I, with the advent of the home refrigerator.

So by these accounts, for the first two hundred and fifty years of American history, the entire nation would have earned a failing grade according to our modern mainstream nutritional advice.

During all this time, however, heart disease was almost certainly rare. Reliable data from death certificates is not available, but other sources of information make a persuasive case against the widespread appearance of the disease before the early 1920s. Austin Flint, the most authoritative expert on heart disease in the United States, scoured the country for reports of heart abnormalities in the mid-1800s, yet reported that he had seen very few cases, despite running a busy practice in New York City. Nor did William Osler, one of the founding professors of Johns Hopkins Hospital, report any cases of heart disease during the 1870s and eighties when working at Montreal General Hospital. The first clinical description of coronary thrombosis came in 1912, and an authoritative textbook in 1915, Diseases of the Arteries including Angina Pectoris , makes no mention at all of coronary thrombosis. On the eve of World War I, the young Paul Dudley White, who later became President Eisenhower’s doctor, wrote that of his seven hundred male patients at Massachusetts General Hospital, only four reported chest pain, “even though there were plenty of them over 60 years of age then.” XI About one fifth of the US population was over fifty years old in 1900. This number would seem to refute the familiar argument that people formerly didn’t live long enough for heart disease to emerge as an observable problem. Simply put, there were some ten million Americans of a prime age for having a heart attack at the turn of the twentieth century, but heart attacks appeared not to have been a common problem.

Was it possible that heart disease existed but was somehow overlooked? The medical historian Leon Michaels compared the record on chest pain with that of two other medical conditions, gout and migraine, which are also painful and episodic and therefore should have been observed by doctors to an equal degree. Michaels catalogs the detailed descriptions of migraines dating all the way back to antiquity; gout, too, was the subject of lengthy notes by doctors and patients alike. Yet chest pain is not mentioned. Michaels therefore finds it “particularly unlikely” that angina pectoris, with its severe, terrifying pain continuing episodically for many years, could have gone unnoticed by the medical community, “if indeed it had been anything but exceedingly rare before the mid-eighteenth century.” XII

So it seems fair to say that at the height of the meat-and-butter-gorging eighteenth and nineteenth centuries, heart disease did not rage as it did by the 1930s. XIII

Ironically—or perhaps tellingly—the heart disease “epidemic” began after a period of exceptionally reduced meat eating. The publication of The Jungle , Upton Sinclair’s fictionalized exposé of the meatpacking industry, caused meat sales in the United States to fall by half in 1906, and they did not revive for another twenty years. In other words, meat eating went down just before coronary disease took off. Fat intake did rise during those years, from 1909 to 1961, when heart attacks surged, but this 12 percent increase in fat consumption was not due to a rise in animal fat. It was instead owing to an increase in the supply of vegetable oils, which had recently been invented.

Nevertheless, the idea that Americans once ate little meat and “mostly plants”—espoused by McGovern and a multitude of experts—continues to endure. And Americans have for decades now been instructed to go back to this earlier, “healthier” diet that seems, upon examination, never to have existed.

A few years ago I jumped into the Dr. Guyenet, Gary Taubes controversy and became actually put off by the categorical, aggressive attitudes from Dr. Guyenet. With time and the more I learn about our metabolism (not least after seriously having read Alberts et al. “Molecular Biology of the CELL” a couple of times) I have turned almost allergic to categorical people (“who know they know”!) in the nutritional field.

That is basically also why I “love” Dr. Kendrick’s blog – very little of these stern attitudes here! Friendly and constructive posts and comments.You learn by reading them all!

E.g. I found the linked video by chris C with the Michael Eades talk above on our topic very rewarding today. Metabolic chemistry to my taste.

I lost all respect for Guyenet when he became a Professional Researcher and deleted a lot of his old blog posts complete with comments. A Real Scientist would have left them and added a commentary as to why his views had changed.

I think most of the work Michael Eades references is in his “protons” series. He is ferociously intelligent and highly knowledgeable and as a vet has not learned what not to think about like a human doctor.

Excellent stuff from Benjamin David Steele above. Now another blog I shall have to read.

I mostly avoid grains, especially wheat, because they spike my blood glucose. I do not have and probably never had a proper Phase 1 insulin response but can still produce a lot of Phase 2 insulin, albeit slowly. Also I used to have horrendous insulin resistance (trigs/HDL nearly 7 and now routinely below 1) so I probably could eat more carbs if I wanted to, but strangely I don’t. It looks like the majority of the population is unable to eat the Government recommended 230 – 300g carbs/day, let alone the 450 – 600g some dieticians recommend, I aim at around 50g, mostly not from grains, others have to eat considerably less but some can eat significantly more.

I notice you did a “posting test” followed by 2 comments split into parts 1 and 2.

Were you having trouble posting comments?

And the reason for splitting your comment? My thought for my posting a comment problem was either (1) something about the link I tried to attach was causing problems or (2) too much text/data in my comment. Which may be the reason for you splitting your comment.

I have not been able to work out how the checkpoints of the passing “system” work. Since my rather extended comment did not pass this time (they often though pass) I tried splitting it and that seemed to work this time.

– several GPs
– a cardiologist
– an endocrinologist
– the FH testing consultant
– a consultant in biochemistry and metabolic, endocrine and nutritional medicine and
– all those “lay” people such as friends and family, who, despite never had a CVD incident, or been on the slab, or having been in intensive care, still reckoned (and reckon) they knew more about it and lectured me and treated me like an idiot to the point that I thought I had either anoxia or hypoxia (which was the concern from the cardiologists upon resuscitation).

Dr Kendrick wrote:
“In truth, the real reason why inflammation is being seen as a possible cause of CVD is because inflammatory markers can be raised in CVD. To my mind this just demonstrates that in people with CVD, lots of damage is occurring, therefore there is more repair going on, so the inflammatory markers are raised.”

I wonder – is there any hope for an anti-inflammatory drug that was targeted on joint cartilage (say), and that would therefore not interfere with the repair of artery walls?

Comfrey cream has worked very well for me when I had a ruptured ACL in my right knee. Also when I was recovering from the operation to replace the ACL in my knee… And I used it after a ligament was torn in my ankle..Both before the op and after.. Now that covers the period 1996 – 2013 I still use it now & then on my knee if it gets sore..

Thanks – and fortunately I don’t need anything of that sort right now – but when I have, it does seem that the internal anti-inflammatories work MUCH better than ointments (disregarding their problems). For example diclofenac has an amazing effect on me, taken as a tablet, but only a tiny effect in the form of Volterol – presumably because so little gets where it is needed.

For those interested in citruline and l-arginine, there is an outfit in Tasmania called “Bulk Nutrients” from whom you can order on the internet by the Kg.(about A$60 for the l-arginine from my last order).

Calcification of plaque in the arteries seems to be one result of the chronic inflammation associated with repeat damage to the endothelium and subsequent repeat healing.
Bone spurs form at the attachment of the plantar aponeurosis (read: plantar fascia) to the heel bone in long distance runners.
It seems that if repeat injury occurs before complete soft tissue healing can take place, the “system” changes gears and reinforces the damaged area with tougher calcification.
If you look at the extreme of calcification, wherein everything turns to bone, you find that inflammation gone wild is an essential part of the syndrome:https://abcnews.go.com/Health/story?id=117774&page=1https://www.ncbi.nlm.nih.gov/pubmed/30429363

I’m wondering how closely related these problems are: Fibrodysplasia ossificans progressiva, osteoarthritis, heel spur, . . . CVD, etc.
Related to vitamin K2 issues perhaps? Something else in common?
We all need a degree of inflammation for proper healing. Is there a way to moderate it?

How closely does the incidence of heart attacks match the areas where, and times when water is chlorinated? Chlorination spread throughout America in the second and third decades of this century, about 20 years before the increase of heart attacks. Light chlorination yielded slow growth of plaques in Price’s cockerels, therefore, chlorination of people’s drinking water at the usual low concentration might have been expected to take at least 10-20 years to produce clinical manifestations of atherosclerosis. http://orthomolecular.org/library/jom/2000/articles/2000-v15n02-p089.shtml

As well as Dr Levy in his multi C protocol, Dr Suzanne Humphries also recommends the Livon Labs liposomal vit C but she also acknowledges its cost and thus perhaps not for mega dosing.

She’s right.

I’ve yet to find any stockist quoting under £30.00 – usually £30.00 to £40.00 range plus shipping. You get 30 sachets in a box, I gram of vit C in a sachet. So, quite expensive.

However, it’s very portable and easy to put in your bag and take to work, especially if you are out and about. Another advantage is that you can also consume it direct from the sachet (it has an orange flavour).

Thanks for the update that the link you provided to Dr Cobb’s website is fixed (or his website is fixed) and I’ve just read his article on reversing heart disease.

Interesting to note that he favours ascorbic acid in preference to mineral ascorbates (such as sodium ascorbate).

I alternate between the two, favouring sodium ascorbate for high dosing, one reason being to minimise the rumbling insides followed by the C flush you always seem to get from doses of ascorbic acid. It’s strong stuff…even when applied topically, which I’ve commented on before but won’t digress here.

His recommendation of about 6 grams in small doses spread out over the day to give maximum coverage thus makes good sense. And avoids the degradation of vitamin C during the course of the day, assuming you take it in powder or crystalline form and just mix one batch. I did find and post some figures from the Vit C Foundation on the degradation of vit c once mixed in water but can’t find them right now.

Charles, It would be nice to see the reference on degradation of vitamin C dissolved in water. I am sipping my 15 g/day in a big glass of water during the day and have noted a slight change of the taste with time so some oxidation is reasonably taking place – but how much?

I know that one is generally cautioning of cooking not to destroy the vitamin but in cold water this must probably be a slow process.

There were a few mentions of this on the Vitamin C Foundation’s forum section.

For example, a discussion called “sodium ascorbate and water” specifically deals with this. Part of Owen Fonorow’s answer included:

“according to Sherry Lewin, all vitamin C breaks down by 50% in about 4 hours in water, but then the concentration remains at 50% for a long period. The higher the concentration of vitamin C, the slower the breakdown.”

No offence, but for those of you who seem intent on blaming modern life, please remember that the biggest problem is the success of it, i.e. longevity. The NHS is being overwhelmed by an ageing population with multiple health conditions. Still I’d rather have this than the good old days when water, food, childbirth, and yes even medicine, weren’t safe.
As for the notion that hunter gatherers were somehow living better lives, I think that is as questionable as it is romantic.
Personally I’d rather live a life that was shorter but highly active. This is of course a personal choice and I remain convinced that the route to it is neither through atorvostatin, nor atavism.

In this, he discusses a few studies, one where they made the LDL-p count really high, and some LDL-p did get through the barrier. In another study (or a part of the same one-I forget), he discusses junction failure and how LDL gets through these. I wonder how well these agree with the post above?

Benjamin, my comment about many ways to get proper nutrients referred to three macronutrients: fats, carbs, proteins and to various food groups that contain them: meats, fruits, vegetables, grains. It wasn’t in relation to raw milk from grass-fed cows vs CAFO cows milk fortified with vitamin D.

Different diet factions have a tendency to single out a particular macronutrient or food group and then pin everything good (or bad) on it. This last sentence doesn’t refer to anything you wrote but to diet wars in general.

I thought I’d ask a question here because I cannot find the answer anywhere, and have been looking for ages. I have just been told by my doctor that my high cholesterol is making my blood thicker than it should be. This means I am at risk, so obviously a statin will sort it all out. Well, she knows I wouldn’t take a statin if it was wrapped in a £20 note, as someone once said on this blog. What I want to know is does cholesterol make your blood thicker. If not, there must presumably be another reason for it.

Complex question in truth. Some people with high cholesterol will also have increased coagulation factors and, yes, statins have an effect on nitric oxide synthesis that can reduce the risk of blood clots. It grinds my teeth to say this, but facts are facts. Are the benefits worth the downsides. In my opinion, no. I think of statins like aspirin. Both drugs can reduce the risk of CVD, both drugs do this through anti-coagulant actions. Both drugs have adverse effects that effectively counteract any potential benefits.

Actually she’s put me on a BP lowering med which. I could see the logic of thicker blood causing my heart to have to do more work to pump thicker blood through my arteries so I reluctantly agreed. I just wondered if cholesterol itself could thickenin the blood. One thing I read somewhere was that being at high altitude can cause this, and a few weeks ago I spent two weeks at the foot of the Himalayas at 7,000 ft. That was dismissed however. Anyway thanks for the reply.

May I ask some somewhat naive questions?
a) is there any correlation either positive or negative between blood lipid levels and cholecystitis?
b) is there any correlation either positive or negative between the prevalence of CVD and gall stones?
c) is there any correlation between CVD and autoimmune disease?

Can only speak for the latter of which I have direct experience. I developed auto immune disease with severe affects on the liver after 5 years on statins. I am now free from statins for up to 8 years having done my research & deciding they were, less say , a poison of the cognitive system and much else.
There are a number of studies linking statins with auto immune including one in the Lancet in 2004 and the followinghttps://www.ncbi.nlm.nih.gov/m/pubmed/23782756/

Wow! I stumbled across this blog doing other research and am blown away. I have read every installment and the logic is impeccable. So now I’m eagerly awaiting the “things you can do to lower your risk” piece. The suspense is killing me, wink wink. Thank you Dr. Kendrick!

Don, I doubt there will be a simple suggestion beyond what has already been written. Stress is a major factor. Vitamin C is a useful thing to have enough of, beyond that it is a matter of using the blog info to carry out research so you understand the factors involved. Mostly, as I see it, it is avoiding the medical industry and looking after yourself. But what do I know? Not a lot, but I don’t care. Life is generally good, low expectations, so few disappointments 10g + vitamin C daily. There are plenty of things other than CVD and MI that will get you, and it suitss me to avoid PUFAs as they are reactive. Read Ray Peat’s site. It has some helpful stuff for me.

Thanks for the reply. I currently get around 20g Vitamin C per day, which I started about a year ago. I think Pauling was on the right track but I’m not hopeful for his vindication, for the reasons Dr. Kendrick points out about the current state of medical research. But you are right, the research is out there for anyone willing to seek it. Good health to you!

Dr. K., The BOOK!!! It arrived yesterday and it’s great. Reading with assiduous (I love that word) attention and much enjoyment.
All the many hours you’ve spent on it. Amazing. Thank you, thank you, thank you.
Happy New Year to you and everyone following this wonderful, educational, enlightening blog.

Hello and thank you for an incredibly informative blog, that I came upon in my ongoing investigations into the reason for my for a high (270) CA CT scan score in the left Coronary artery and (34) in the right.
In addition to your ‘non exhaustive list of causes” above, would I be wise to continue my investigations into these additional causes –
a diagnosis of undiagnosed and untreated Rheumatic Fever with a resulting a damaged incompetent mitral valve, aged 21.
a physical chest injury also aged about 21
the effects of being a semi professional athlete from 17 – 34 yrs old
Rouleaux blood. I am about to have my Fibrinogen levels checked.
I am a fit 62 female with not other conditions/ illnesses or medications and nothing, besides a slightly raised total cholesterol and LDL, that makes me predisposed to CAD.
thank you

Association of All-Cause and Cardiovascular Mortality With High Levels of Physical Activity and Concurrent Coronary Artery Calcification.
In this observational study of 21 758 men with varying levels of physical activity, the presence of elevated levels of coronary artery calcification (≥100 Agatston units) was more prevalent among highly active men. However, no increase in all-cause or cardiovascular disease mortality was evident in this group when compared with men who were less active.https://jamanetwork.com/journals/jamacardiology/fullarticle/2722746?

I wondered who else would notice that. Interesting. Calcification was increased in those who exercised a lot, but no correction with CVD. It seems that you can have both good, and bad, calcification. What to make of that, I wonder?

The development of atherosclerotic plaques typically occurs in regions of arteries that have disturbed blood flow. While blood flow disturbances are known to alter endothelial gene expression and function, it is not clear how altered blood flow induces these changes.
Evidence that blood flow disturbances alter genome-wide methylation patterns in endothelial cells through induction of the DNA methyltransferase DNMT. Long-term epigenetic changes induced within the arterial endothelium may lead to development of atherosclerosis, and genes that are altered in response to disturbed flow represent potential therapeutic targets for limiting plaque formation.

Dr. Kendrick – thanks for a great post. I learned a lot. I wonder what’s your response to Ivor Cummins’ counter explanation of Transcytosis: how LDL traverses through the endothelial cells, as well as in between them. https://www.youtube.com/watch?v=vBKa6d6j9_8

He continues to dispute that LDL does not pass the BBB (min 15) – by quoting from “A new function for the LDL receptor: transcytosis of LDL across the blood-brain barrier.” (https://www.ncbi.nlm.nih.gov/pubmed/9265653)

This full explanation is informative and extremely helpful. I know high BP is a risk factor for heart disease. But my question is what categorises ‘high’
Does it depend on age – as in the elderly (75-80) blood pressure that would be considered high in young age is not the same in elderly. Is this correct? and is trying to lower it with medication in the elderly
a mistake because of drug side effects. ?

Mr Chris: Like Dr. Kendrick, I don’t know what my BP is, and I don’t want to know. But, I had to get a new doctor due to a persistent problem. I allowed it to be taken. 160/80. This didn’t please me, but I had made a photocopy copy of Port, et al, and handed it to the doctor. The 160 is at the top of the high normal range for my age. I am not concerned, as I think part of the reason is white coat syndrome. The good news is that I really like my new doctor. She, and the whole staff are really low key. This is what I like. I don’t like it when people have a fit over problems that need to be solved. Just get on with it.

Interesting……””Against the predictions of the linear logistic model, neither all-cause nor cardiovascular deaths depended on systolic blood pressure in a strictly increasing manner. The linear logistic model was rejected by the Framingham data. Instead, risk was independent of systolic blood pressure for all pressures lower than a threshold at the 70th percentile for a person of a given age and sex. Risk sharply increased with pressure higher than the 80th percentile.””

Seems to be saying that the establishment’s drive to get systolic below 140 at all costs is misplaced.

Dr Kendrick cannot provide individual patient advice over the Internet. UK General Medical Council regulations are clear that to do so would be a breach of medical standards that could result in disciplinary proceedings.

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